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Santa Cruz Biotechnology sox2 sirna human

Confirmation of siRNA-mediated KD of NES expression in Panc1 cell variants and <t>SOX2</t> expression in Panc89 cell variants. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 cell variants, SOX2 in Panc89 cell variants and double KD of NES/SOX2 in all cell variants or to CTRLsi transfection for 72 h. Afterward, the KD was confirmed by RT-qPCR (a, c, e, g) and IFS (b, d, f, h). Every analysis was performed with n = 3 independent experiments. Gene expression data of NES and SOX2 (a, c, e, g) are normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test, followed by one-way ANOVA for statistical significance. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. Data are presented by mean with SD. Representative IFS images from n = 3 independent experiments are shown (b, d, f, h). Scale bars IFS = 1000 μm. (KD = knockdown; RT-qPCR = real time quantitative polymerase chain reaction, IFS = immunofluorescence staining, CTRLsi = control siRNA; SD = standard deviation; Holo = Holoclone)

Sox2 Sirna Human, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 21 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 93 stars, based on 21 article reviews

sox2 sirna human - by Bioz Stars, 2026-09

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1) Product Images from "Nestin and SOX2 Maintain self-renewal Abilities of Different Pancreatic Cancer Stem Cell Populations"

Article Title: Nestin and SOX2 Maintain self-renewal Abilities of Different Pancreatic Cancer Stem Cell Populations

Journal: Stem Cell Reviews and Reports

doi: 10.1007/s12015-025-11006-3

Confirmation of siRNA-mediated KD of NES expression in Panc1 cell variants and SOX2 expression in Panc89 cell variants. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 cell variants, SOX2 in Panc89 cell variants and double KD of NES/SOX2 in all cell variants or to CTRLsi transfection for 72 h. Afterward, the KD was confirmed by RT-qPCR (a, c, e, g) and IFS (b, d, f, h). Every analysis was performed with n = 3 independent experiments. Gene expression data of NES and SOX2 (a, c, e, g) are normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test, followed by one-way ANOVA for statistical significance. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. Data are presented by mean with SD. Representative IFS images from n = 3 independent experiments are shown (b, d, f, h). Scale bars IFS = 1000 μm. (KD = knockdown; RT-qPCR = real time quantitative polymerase chain reaction, IFS = immunofluorescence staining, CTRLsi = control siRNA; SD = standard deviation; Holo = Holoclone)

Figure Legend Snippet: Confirmation of siRNA-mediated KD of NES expression in Panc1 cell variants and SOX2 expression in Panc89 cell variants. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 cell variants, SOX2 in Panc89 cell variants and double KD of NES/SOX2 in all cell variants or to CTRLsi transfection for 72 h. Afterward, the KD was confirmed by RT-qPCR (a, c, e, g) and IFS (b, d, f, h). Every analysis was performed with n = 3 independent experiments. Gene expression data of NES and SOX2 (a, c, e, g) are normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test, followed by one-way ANOVA for statistical significance. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. Data are presented by mean with SD. Representative IFS images from n = 3 independent experiments are shown (b, d, f, h). Scale bars IFS = 1000 μm. (KD = knockdown; RT-qPCR = real time quantitative polymerase chain reaction, IFS = immunofluorescence staining, CTRLsi = control siRNA; SD = standard deviation; Holo = Holoclone)

Techniques Used: Expressing, Transfection, Quantitative RT-PCR, Gene Expression, Knockdown, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Control, Standard Deviation

Gene expression analysis of EMT markers and plasticity modulators after single and double KD of NES and SOX2 in Panc1 and Panc89 cell variants. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 cell variants (a), SOX2 in Panc89 cell variants (c), double KD of NES/SOX2 in Panc1 cell variants (b) and Panc89 cell variants (d) or to CTRLsi transfection (a-d) for 72 h. Afterward, gene expression of EMT markers (a-d top: CDH1 , L1CAM , VIM ) and plasticity modulators (a-d bottom: ZEB1 , ZEB2 , OVOL2 ) was determined via RT-qPCR. Analysis was performed with n = 3 independent experiments. Gene expression data of all genes of interest were first normalized to the reference gene GAPDH and then normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test. Parametric data were tested by one-way ANOVA and are presented by mean with SD. Non-parametric data were tested by Kruskal-Wallis one-way ANOVA on ranks and are presented as median with interquartile range. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. (CSC = cancer stem cell; EMT = Epithelial-to-Mesenchymal Transition; KD = knockdown; RT-qPCR = real time quantitative polymerase chain reaction; CTRLsi = control siRNA; SD = standard deviation; Holo = Holoclone)

Figure Legend Snippet: Gene expression analysis of EMT markers and plasticity modulators after single and double KD of NES and SOX2 in Panc1 and Panc89 cell variants. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 cell variants (a), SOX2 in Panc89 cell variants (c), double KD of NES/SOX2 in Panc1 cell variants (b) and Panc89 cell variants (d) or to CTRLsi transfection (a-d) for 72 h. Afterward, gene expression of EMT markers (a-d top: CDH1 , L1CAM , VIM ) and plasticity modulators (a-d bottom: ZEB1 , ZEB2 , OVOL2 ) was determined via RT-qPCR. Analysis was performed with n = 3 independent experiments. Gene expression data of all genes of interest were first normalized to the reference gene GAPDH and then normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test. Parametric data were tested by one-way ANOVA and are presented by mean with SD. Non-parametric data were tested by Kruskal-Wallis one-way ANOVA on ranks and are presented as median with interquartile range. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. (CSC = cancer stem cell; EMT = Epithelial-to-Mesenchymal Transition; KD = knockdown; RT-qPCR = real time quantitative polymerase chain reaction; CTRLsi = control siRNA; SD = standard deviation; Holo = Holoclone)

Techniques Used: Gene Expression, Transfection, Quantitative RT-PCR, Knockdown, Real-time Polymerase Chain Reaction, Control, Standard Deviation

KD of NES in Panc1 cell variants and KD of SOX2 in Panc89 cell variants marginally impact cell growth but significantly decrease self-renewing properties. 5 × 10 4 cells were either left untreated (a) or were subjected to siRNA-mediated KD of NES in Panc1 cell variants (b, d), SOX2 in Panc89 cell variants (c, e), double KD of NES/SOX2 in all cell variants (c-e) or to CTRLsi transfection (b-e) for 72 h. Afterward, the number of viable cells was determined by Trypan blue staining (a-c) and cells were re-seeded with 400 cells/well for Panc1 cell variants or 200 cells/well for Panc89 cell variants for CFA in 12-well plates (d-e). The number of viable cells under KD of NES (b), SOX2 (b) or NES / SOX2 (c) was normalized to CTRLsi conditions. Data were tested for normal distribution by Shapiro-Wilk analysis, followed by one-way ANOVA and Tukey´s multiple comparison test. d-e) CFAs were monitored for 6–10 d, fixed with PFA and stained with crystal violet. CFA data were analyzed by two-way ANOVA and Tukey´s multiple comparison. Every analysis was performed with n = 3 independent experiments plus technical replicates and data are shown as mean with SEM. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. (KD = knockdown; CTRLsi = control siRNA; CFA = colony formation assay; SEM = standard error of means; Holo = Holoclone; PFA = paraformaldehyde; SEM = standard error of means; Holo = Holoclone; No. = Number; w/o KD = without knockdown)

Figure Legend Snippet: KD of NES in Panc1 cell variants and KD of SOX2 in Panc89 cell variants marginally impact cell growth but significantly decrease self-renewing properties. 5 × 10 4 cells were either left untreated (a) or were subjected to siRNA-mediated KD of NES in Panc1 cell variants (b, d), SOX2 in Panc89 cell variants (c, e), double KD of NES/SOX2 in all cell variants (c-e) or to CTRLsi transfection (b-e) for 72 h. Afterward, the number of viable cells was determined by Trypan blue staining (a-c) and cells were re-seeded with 400 cells/well for Panc1 cell variants or 200 cells/well for Panc89 cell variants for CFA in 12-well plates (d-e). The number of viable cells under KD of NES (b), SOX2 (b) or NES / SOX2 (c) was normalized to CTRLsi conditions. Data were tested for normal distribution by Shapiro-Wilk analysis, followed by one-way ANOVA and Tukey´s multiple comparison test. d-e) CFAs were monitored for 6–10 d, fixed with PFA and stained with crystal violet. CFA data were analyzed by two-way ANOVA and Tukey´s multiple comparison. Every analysis was performed with n = 3 independent experiments plus technical replicates and data are shown as mean with SEM. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. (KD = knockdown; CTRLsi = control siRNA; CFA = colony formation assay; SEM = standard error of means; Holo = Holoclone; PFA = paraformaldehyde; SEM = standard error of means; Holo = Holoclone; No. = Number; w/o KD = without knockdown)

Techniques Used: Transfection, Staining, Comparison, Knockdown, Control, Colony Assay

siRNA-mediated KD of NES in Panc1 and SOX2 in Panc89 cell variants marginally impacts migration and invasion properties. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 and SOX2 Panc89 cell variants or to CTRLsi transfection for 72 h. Afterward, transfected cells were detached and seeded in (a) Ibidi ® 2-well culture inserts (4 × 10 4 for Panc1; 3 × 10 4 for Panc89 cell variants) and migration was analyzed after 24 h for Panc1 and Panc89 cell variants, or in (b) 96-well ULA plates for spheroid formation (1 × 10 4 for Panc1 cell variants; 1.5 × 10 4 for Panc89 cell variants) and determination of invasion properties. Cell invasion (number of invasive fronts [#]; invasion distance [µm]) was analyzed after 72 and 120 h for Panc1 and Panc89 cell variants, respectively. Every analysis was performed with n = 3 independent experiments plus technical replicates and NES and SOX2 KD values, respectively, were normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test. Parametric data were tested by one-way ANOVA with Tukey´s multiple comparison and are presented by mean with SEM. Non-parametric data were tested by Kruskal-Wallis one-way ANOVA on ranks and are presented as median with interquartile range. Representative images from n = 3 independent experiments are shown (a, b; top). Scale bar a) = 200 μm, b) left = 400 μm, b) right = 200 μm. (KD = knockdown; CTRLsi = control siRNA; ULA = ultra-low-attachment plate; SEM = standard error of means; Holo = Holoclone)

Figure Legend Snippet: siRNA-mediated KD of NES in Panc1 and SOX2 in Panc89 cell variants marginally impacts migration and invasion properties. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 and SOX2 Panc89 cell variants or to CTRLsi transfection for 72 h. Afterward, transfected cells were detached and seeded in (a) Ibidi ® 2-well culture inserts (4 × 10 4 for Panc1; 3 × 10 4 for Panc89 cell variants) and migration was analyzed after 24 h for Panc1 and Panc89 cell variants, or in (b) 96-well ULA plates for spheroid formation (1 × 10 4 for Panc1 cell variants; 1.5 × 10 4 for Panc89 cell variants) and determination of invasion properties. Cell invasion (number of invasive fronts [#]; invasion distance [µm]) was analyzed after 72 and 120 h for Panc1 and Panc89 cell variants, respectively. Every analysis was performed with n = 3 independent experiments plus technical replicates and NES and SOX2 KD values, respectively, were normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test. Parametric data were tested by one-way ANOVA with Tukey´s multiple comparison and are presented by mean with SEM. Non-parametric data were tested by Kruskal-Wallis one-way ANOVA on ranks and are presented as median with interquartile range. Representative images from n = 3 independent experiments are shown (a, b; top). Scale bar a) = 200 μm, b) left = 400 μm, b) right = 200 μm. (KD = knockdown; CTRLsi = control siRNA; ULA = ultra-low-attachment plate; SEM = standard error of means; Holo = Holoclone)

Techniques Used: Migration, Transfection, Comparison, Knockdown, Control

siRNA-mediated KD of NES in Panc1 cell variants and SOX2 in Panc89 cell variants marginally impacts the response to cytostatic drugs. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 and SOX2 Panc89 cell variants or to CTRLsi transfection for 72 h. Afterward, 1 × 10 3 cells/well of either cell variants and conditions were re-seeded in a 96-well plate and after 24 h, the cells were treated with Gemcitabine, 5-FU or Oxaliplatin for 72 h. Then, (a) Panc1 and (b) Panc89 cell variants were stained with Hoechst 33342 (1:5000) and PI (1:50) and imaged to determine the total number of cells (Hoechst-positive, nuclei count) and the number of dead cells (Hoechst/PI-positive, cell death), respectively. Every analysis was performed with n = 3 independent experiments. The nuclei count and cell death values after KD of NES and SOX2 , respectively, were normalized to CTRLsi conditions. All data sets were analyzed by two-way ANOVA and Tukey´s multiple comparison. Every analysis was performed with n = 3 independent experiments plus technical replicates and data are shown as mean with SEM. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. (KD = knockdown; CTRLsi = control siRNA; 5-FU = 5-Fluorouracil; PI = propidium iodide; SEM = standard error of means; Holo = Holoclone)

Figure Legend Snippet: siRNA-mediated KD of NES in Panc1 cell variants and SOX2 in Panc89 cell variants marginally impacts the response to cytostatic drugs. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 and SOX2 Panc89 cell variants or to CTRLsi transfection for 72 h. Afterward, 1 × 10 3 cells/well of either cell variants and conditions were re-seeded in a 96-well plate and after 24 h, the cells were treated with Gemcitabine, 5-FU or Oxaliplatin for 72 h. Then, (a) Panc1 and (b) Panc89 cell variants were stained with Hoechst 33342 (1:5000) and PI (1:50) and imaged to determine the total number of cells (Hoechst-positive, nuclei count) and the number of dead cells (Hoechst/PI-positive, cell death), respectively. Every analysis was performed with n = 3 independent experiments. The nuclei count and cell death values after KD of NES and SOX2 , respectively, were normalized to CTRLsi conditions. All data sets were analyzed by two-way ANOVA and Tukey´s multiple comparison. Every analysis was performed with n = 3 independent experiments plus technical replicates and data are shown as mean with SEM. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. (KD = knockdown; CTRLsi = control siRNA; 5-FU = 5-Fluorouracil; PI = propidium iodide; SEM = standard error of means; Holo = Holoclone)

Techniques Used: Transfection, Staining, Comparison, Knockdown, Control

other:

Article Title: Glucocorticoids inhibit the maturation of committed osteoblasts via SOX2.
Article Snippet: Antibodies against RUNX2, RANKL, and SOX2 (sc-365823), SOX2 siRNA, and scrambled siRNA (Si-scr) were purchased from Santa Cruz Biotechnology.

Article Title: Chromium (VI)‐induced ALDH1A1/EGF axis promotes lung cancer progression
Article Snippet: DACH1 siRNA (sc‐77089), ABCB5 siRNA (sc‐89856), MERTK siRNA (sc‐37127), KLF4 siRNA (sc‐35480), SOX2 siRNA (sc‐38408), EGF siRNA (sc‐39416), and ALDH1A1 siRNA (sc‐41442) were purchased from Santa Cruz Biotechnology (CA, USA).

Transfection:

Article Title: Transcription factor SOX2 contributes to nonalcoholic fatty liver disease development by regulating the expression of the fatty acid transporter CD36.
Article Snippet: .. FL83B cells at a density of 1 9 105 per well in a 12-well dish were transfected with Sox2 siRNA (si-SOX2), scrambled siRNA (si-Scr; Santa Cruz Biotechnology), pLNCX2-SOX2 (SOX2), or the pLNCX2 vector (pLNCX2) using lipofectamine 3000 reagent (Invitrogen), according to the manufacturer’s instructions. ..

Article Title: Sox2 contributes to tooth development via Wnt signaling.
Article Snippet: The transcription factor Sox2 is a stem cell marker that dictates cell lineage.. It has been shown to mark the epithelial stem cells of the continuously growingmouse incisors.. Sox2 also interferes with Wnt signaling by binding to β-catenin, a central mediator of the Wnt pathway.

Article Title: SOX2 is a positive regulator of osteoclast differentiation.
Article Snippet: Elucidating the mechanism underlying osteoclast differentiation is important to improve our understanding of the pathophysiologies related to skeletal diseases and osteolytic metastasis in cancer.. Sexdetermining region Y-box containing gene 2 (SOX2), a stemness marker, is known to affect osteoblast differentiation and cancer metastasis.. However, its role in osteoclastogenesis has not been investigated to date.

Article Title: Distinct transcriptional programs of SOX2 in different types of small cell lung cancers
Article Snippet: .. We purchased Sox2 siRNA (sc-41120) and Ascl1 siRNA (sc-37692) from Santa Cruz Biotechnology (Santa Cruz, USA) and transfected them into cells using an electroporator (NEPA21 pulse generator; Nepa Gene, Chiba, Japan) as described in the manufacturer’s instructions. ..

Plasmid Preparation:

Control:

Article Title: Cationic lipoplexes for treatment of cancer stem cell-derived murine lung tumors
Article Snippet: .. Control and SOX2 siRNA were purchased from Santa Cruz Biotechnology (Santa Cruz, CA). ..

Image Search Results

Journal: Stem Cell Reviews and Reports

Article Title: Nestin and SOX2 Maintain self-renewal Abilities of Different Pancreatic Cancer Stem Cell Populations

doi: 10.1007/s12015-025-11006-3

Figure Lengend Snippet: Confirmation of siRNA-mediated KD of NES expression in Panc1 cell variants and SOX2 expression in Panc89 cell variants. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 cell variants, SOX2 in Panc89 cell variants and double KD of NES/SOX2 in all cell variants or to CTRLsi transfection for 72 h. Afterward, the KD was confirmed by RT-qPCR (a, c, e, g) and IFS (b, d, f, h). Every analysis was performed with n = 3 independent experiments. Gene expression data of NES and SOX2 (a, c, e, g) are normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test, followed by one-way ANOVA for statistical significance. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. Data are presented by mean with SD. Representative IFS images from n = 3 independent experiments are shown (b, d, f, h). Scale bars IFS = 1000 μm. (KD = knockdown; RT-qPCR = real time quantitative polymerase chain reaction, IFS = immunofluorescence staining, CTRLsi = control siRNA; SD = standard deviation; Holo = Holoclone)

Article Snippet: SOX2 siRNA (human) (sc-38408) , 10 , Santa Cruz Biotechnology, Texas, US.

Techniques: Expressing, Transfection, Quantitative RT-PCR, Gene Expression, Knockdown, Real-time Polymerase Chain Reaction, Immunofluorescence, Staining, Control, Standard Deviation

Journal: Stem Cell Reviews and Reports

Article Title: Nestin and SOX2 Maintain self-renewal Abilities of Different Pancreatic Cancer Stem Cell Populations

doi: 10.1007/s12015-025-11006-3

Figure Lengend Snippet: Gene expression analysis of EMT markers and plasticity modulators after single and double KD of NES and SOX2 in Panc1 and Panc89 cell variants. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 cell variants (a), SOX2 in Panc89 cell variants (c), double KD of NES/SOX2 in Panc1 cell variants (b) and Panc89 cell variants (d) or to CTRLsi transfection (a-d) for 72 h. Afterward, gene expression of EMT markers (a-d top: CDH1 , L1CAM , VIM ) and plasticity modulators (a-d bottom: ZEB1 , ZEB2 , OVOL2 ) was determined via RT-qPCR. Analysis was performed with n = 3 independent experiments. Gene expression data of all genes of interest were first normalized to the reference gene GAPDH and then normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test. Parametric data were tested by one-way ANOVA and are presented by mean with SD. Non-parametric data were tested by Kruskal-Wallis one-way ANOVA on ranks and are presented as median with interquartile range. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. (CSC = cancer stem cell; EMT = Epithelial-to-Mesenchymal Transition; KD = knockdown; RT-qPCR = real time quantitative polymerase chain reaction; CTRLsi = control siRNA; SD = standard deviation; Holo = Holoclone)

Article Snippet: SOX2 siRNA (human) (sc-38408) , 10 , Santa Cruz Biotechnology, Texas, US.

Techniques: Gene Expression, Transfection, Quantitative RT-PCR, Knockdown, Real-time Polymerase Chain Reaction, Control, Standard Deviation

Journal: Stem Cell Reviews and Reports

Article Title: Nestin and SOX2 Maintain self-renewal Abilities of Different Pancreatic Cancer Stem Cell Populations

doi: 10.1007/s12015-025-11006-3

Figure Lengend Snippet: KD of NES in Panc1 cell variants and KD of SOX2 in Panc89 cell variants marginally impact cell growth but significantly decrease self-renewing properties. 5 × 10 4 cells were either left untreated (a) or were subjected to siRNA-mediated KD of NES in Panc1 cell variants (b, d), SOX2 in Panc89 cell variants (c, e), double KD of NES/SOX2 in all cell variants (c-e) or to CTRLsi transfection (b-e) for 72 h. Afterward, the number of viable cells was determined by Trypan blue staining (a-c) and cells were re-seeded with 400 cells/well for Panc1 cell variants or 200 cells/well for Panc89 cell variants for CFA in 12-well plates (d-e). The number of viable cells under KD of NES (b), SOX2 (b) or NES / SOX2 (c) was normalized to CTRLsi conditions. Data were tested for normal distribution by Shapiro-Wilk analysis, followed by one-way ANOVA and Tukey´s multiple comparison test. d-e) CFAs were monitored for 6–10 d, fixed with PFA and stained with crystal violet. CFA data were analyzed by two-way ANOVA and Tukey´s multiple comparison. Every analysis was performed with n = 3 independent experiments plus technical replicates and data are shown as mean with SEM. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. (KD = knockdown; CTRLsi = control siRNA; CFA = colony formation assay; SEM = standard error of means; Holo = Holoclone; PFA = paraformaldehyde; SEM = standard error of means; Holo = Holoclone; No. = Number; w/o KD = without knockdown)

Article Snippet: SOX2 siRNA (human) (sc-38408) , 10 , Santa Cruz Biotechnology, Texas, US.

Techniques: Transfection, Staining, Comparison, Knockdown, Control, Colony Assay

Journal: Stem Cell Reviews and Reports

Article Title: Nestin and SOX2 Maintain self-renewal Abilities of Different Pancreatic Cancer Stem Cell Populations

doi: 10.1007/s12015-025-11006-3

Figure Lengend Snippet: siRNA-mediated KD of NES in Panc1 and SOX2 in Panc89 cell variants marginally impacts migration and invasion properties. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 and SOX2 Panc89 cell variants or to CTRLsi transfection for 72 h. Afterward, transfected cells were detached and seeded in (a) Ibidi ® 2-well culture inserts (4 × 10 4 for Panc1; 3 × 10 4 for Panc89 cell variants) and migration was analyzed after 24 h for Panc1 and Panc89 cell variants, or in (b) 96-well ULA plates for spheroid formation (1 × 10 4 for Panc1 cell variants; 1.5 × 10 4 for Panc89 cell variants) and determination of invasion properties. Cell invasion (number of invasive fronts [#]; invasion distance [µm]) was analyzed after 72 and 120 h for Panc1 and Panc89 cell variants, respectively. Every analysis was performed with n = 3 independent experiments plus technical replicates and NES and SOX2 KD values, respectively, were normalized to CTRLsi conditions. All data sets were tested for normal distribution using Shapiro-Wilk test. Parametric data were tested by one-way ANOVA with Tukey´s multiple comparison and are presented by mean with SEM. Non-parametric data were tested by Kruskal-Wallis one-way ANOVA on ranks and are presented as median with interquartile range. Representative images from n = 3 independent experiments are shown (a, b; top). Scale bar a) = 200 μm, b) left = 400 μm, b) right = 200 μm. (KD = knockdown; CTRLsi = control siRNA; ULA = ultra-low-attachment plate; SEM = standard error of means; Holo = Holoclone)

Article Snippet: SOX2 siRNA (human) (sc-38408) , 10 , Santa Cruz Biotechnology, Texas, US.

Techniques: Migration, Transfection, Comparison, Knockdown, Control

Journal: Stem Cell Reviews and Reports

Article Title: Nestin and SOX2 Maintain self-renewal Abilities of Different Pancreatic Cancer Stem Cell Populations

doi: 10.1007/s12015-025-11006-3

Figure Lengend Snippet: siRNA-mediated KD of NES in Panc1 cell variants and SOX2 in Panc89 cell variants marginally impacts the response to cytostatic drugs. 5 × 10 4 cells were subjected to siRNA-mediated KD of NES in Panc1 and SOX2 Panc89 cell variants or to CTRLsi transfection for 72 h. Afterward, 1 × 10 3 cells/well of either cell variants and conditions were re-seeded in a 96-well plate and after 24 h, the cells were treated with Gemcitabine, 5-FU or Oxaliplatin for 72 h. Then, (a) Panc1 and (b) Panc89 cell variants were stained with Hoechst 33342 (1:5000) and PI (1:50) and imaged to determine the total number of cells (Hoechst-positive, nuclei count) and the number of dead cells (Hoechst/PI-positive, cell death), respectively. Every analysis was performed with n = 3 independent experiments. The nuclei count and cell death values after KD of NES and SOX2 , respectively, were normalized to CTRLsi conditions. All data sets were analyzed by two-way ANOVA and Tukey´s multiple comparison. Every analysis was performed with n = 3 independent experiments plus technical replicates and data are shown as mean with SEM. Significances are indicated by asterisk: p ≤ 0.033 = *, p ≤ 0.002 = **, p ≤ 0.001 = ***. (KD = knockdown; CTRLsi = control siRNA; 5-FU = 5-Fluorouracil; PI = propidium iodide; SEM = standard error of means; Holo = Holoclone)

Article Snippet: SOX2 siRNA (human) (sc-38408) , 10 , Santa Cruz Biotechnology, Texas, US.

Techniques: Transfection, Staining, Comparison, Knockdown, Control

The expression of TGIF2 and SOX2 in human PC and adjacent pancreas. A. TGIF2 and SOX2 expression in PC and paired pancreas specimens by IHC. B and C. TGIF2, SOX2, EGFR and E-cad expression in two PC specimens (#21 and #37). D. The mRNA level of TGIF2 in 20 cases of human PC and adjacent pancreas by qRT-PCR (T: PC; N: paired pancreas) and SOX2. E. The mRNA level of SOX2 in our cohort. F and G. High and low expression of TGIF2 and SOX2 against prognosis. H. Combination of TGIF2 and SOX2 against prognosis.

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: The expression of TGIF2 and SOX2 in human PC and adjacent pancreas. A. TGIF2 and SOX2 expression in PC and paired pancreas specimens by IHC. B and C. TGIF2, SOX2, EGFR and E-cad expression in two PC specimens (#21 and #37). D. The mRNA level of TGIF2 in 20 cases of human PC and adjacent pancreas by qRT-PCR (T: PC; N: paired pancreas) and SOX2. E. The mRNA level of SOX2 in our cohort. F and G. High and low expression of TGIF2 and SOX2 against prognosis. H. Combination of TGIF2 and SOX2 against prognosis.

Article Snippet: The siRNA and shRNA sequences for TGIF2 and SOX2 were summarized in , which were synthesized by GenePharma Co., Ltd. (Shanghai, China). shRNA-mediated TGIF2 and SOX2 silencing and lentivirus vector (GV492 and CV186)-mediated TGIF2, SOX2, and Smad2 overexpression (TGIF2-OE, SOX2-OE, and Smad2-OE, respectively) were purchased from GeneChem (Shanghai, China). siRNAs and plasmids were mixed with Oligofectamine 3000 (Invitrogen, Carlsbad, CA, USA) according to the manufacturer's instructions.

Techniques: Expressing, Quantitative RT-PCR

The relationship among TGIF2, SOX2, EGFR and E-cad expression in 88 cases of clinical PC samples

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: The relationship among TGIF2, SOX2, EGFR and E-cad expression in 88 cases of clinical PC samples

Techniques: Expressing

Univariate and Multivariate analysis in survival time

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: Univariate and Multivariate analysis in survival time

Techniques:

Coordination of TGIF2/SOX2 promotes EMT of PC in vitro . A and B. TGIF2 and SOX2 protein (A) and mRNA (B) level in 4 PC cell lines. C. The protein expression of TGIF2, SOX2 and EMT signaling in Scramble, TGIF2-OE, siSOX2 and TGIF2-OE/siSOX2 groups in PANC-1 cells. D. The protein expression of TGIF2, SOX2 and EMT signaling in Scramble, siTGIF2, SOX2-OE, and siTGIF2/SOX2-OE groups in BxPC-3 cells. E. The EMT phenotype in Scramble, TGIF2-OE, siSOX2 and TGIF2-OE/siSOX2 groups in PANC-1 cells. F. The EMT phenotype in Scramble, SOX2-OE, siTGIF2 and siTGIF2/SOX2-OE groups in BxPC-3 cells. G and H. Cell invasion (G) and migration (H) in Scramble, TGIF2-OE, siSOX2 and TGIF2-OE/siSOX2 groups in PANC-1 cells. I and J. Cell invasion (I) and migration (J) in Scramble, siTGIF2, SOX2-OE and siTGIF2/SOX2-OE groups Scramble, SOX2-OE, siTGIF2 and siTGIF2/SOX2-OE in BxPC-3 cells. Bars indicate ± S.E.*, P <0.05; **, P <0.01 compared with the control.

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: Coordination of TGIF2/SOX2 promotes EMT of PC in vitro . A and B. TGIF2 and SOX2 protein (A) and mRNA (B) level in 4 PC cell lines. C. The protein expression of TGIF2, SOX2 and EMT signaling in Scramble, TGIF2-OE, siSOX2 and TGIF2-OE/siSOX2 groups in PANC-1 cells. D. The protein expression of TGIF2, SOX2 and EMT signaling in Scramble, siTGIF2, SOX2-OE, and siTGIF2/SOX2-OE groups in BxPC-3 cells. E. The EMT phenotype in Scramble, TGIF2-OE, siSOX2 and TGIF2-OE/siSOX2 groups in PANC-1 cells. F. The EMT phenotype in Scramble, SOX2-OE, siTGIF2 and siTGIF2/SOX2-OE groups in BxPC-3 cells. G and H. Cell invasion (G) and migration (H) in Scramble, TGIF2-OE, siSOX2 and TGIF2-OE/siSOX2 groups in PANC-1 cells. I and J. Cell invasion (I) and migration (J) in Scramble, siTGIF2, SOX2-OE and siTGIF2/SOX2-OE groups Scramble, SOX2-OE, siTGIF2 and siTGIF2/SOX2-OE in BxPC-3 cells. Bars indicate ± S.E.*, P <0.05; **, P <0.01 compared with the control.

Techniques: In Vitro, Expressing, Migration, Control

Coordination of TGIF2/SOX2 promotes CSCs and drug resistance of PC in vitro . A and B. Sphere formation in PANC-1 cells (A) and BxPC-3 (B) cells following the activation of TGIF2, SOX2, CD133, CD44 and EGFR/MAPK signaling. C and D. The sphere number (C) and the protein expression of TGIF2, SOX2, CD133, CD44 and EGFR/MAPK signaling (D) in Scramble, TGIF2-OE, siSOX2 and TGIF2-OE/siSOX2 groups in PANC-1 cells. E and F The sphere number (E) and the protein expression of TGIF2, SOX2, CD133, CD44 and EGFR/MAPK signaling (F) in Scramble, siTGIF2, SOX2-OE and siTGIF2/SOX2-OE groups in BxPC-3 cells. ( G-H ) the spheroids number of PC in wildtype (treated with EGF to activate EGFR/ERK signaling) and Kras-mutant (constant activation of EGFR/ERK signaling) mice. ( I ) The overexpression of TGIF2, SOX2, CD133 and p-ERK were in pancreatic intraepithelial neoplasia (PanIN) of KC mice. J. Cell growth in Scramble, TGIF2-OE, siSOX2, TGIF2-OE/siSOX2 and TGIF2-OE/Erlotinib groups of PANC-1 cells and in Scramble, siTGIF2, SOX2-OE and siTGIF2/SOX2-OE of BxPC-3 cells by MTT. K. Under various concentration of Gemcitabine treatment, Cell proliferation rate in Scramble, TGIF2-OE, siSOX2, TGIF2-OE/siSOX2 and TGIF2-OE/Erlotinib groups of PANC-1 cells and in Scramble, siTGIF2, SOX2-OE and siTGIF2/SOX2-OE of BxPC-3 cells by MTT. Bars indicate ± S.E.*, P <0.05; **, P <0.01 compared with the control.

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: Coordination of TGIF2/SOX2 promotes CSCs and drug resistance of PC in vitro . A and B. Sphere formation in PANC-1 cells (A) and BxPC-3 (B) cells following the activation of TGIF2, SOX2, CD133, CD44 and EGFR/MAPK signaling. C and D. The sphere number (C) and the protein expression of TGIF2, SOX2, CD133, CD44 and EGFR/MAPK signaling (D) in Scramble, TGIF2-OE, siSOX2 and TGIF2-OE/siSOX2 groups in PANC-1 cells. E and F The sphere number (E) and the protein expression of TGIF2, SOX2, CD133, CD44 and EGFR/MAPK signaling (F) in Scramble, siTGIF2, SOX2-OE and siTGIF2/SOX2-OE groups in BxPC-3 cells. ( G-H ) the spheroids number of PC in wildtype (treated with EGF to activate EGFR/ERK signaling) and Kras-mutant (constant activation of EGFR/ERK signaling) mice. ( I ) The overexpression of TGIF2, SOX2, CD133 and p-ERK were in pancreatic intraepithelial neoplasia (PanIN) of KC mice. J. Cell growth in Scramble, TGIF2-OE, siSOX2, TGIF2-OE/siSOX2 and TGIF2-OE/Erlotinib groups of PANC-1 cells and in Scramble, siTGIF2, SOX2-OE and siTGIF2/SOX2-OE of BxPC-3 cells by MTT. K. Under various concentration of Gemcitabine treatment, Cell proliferation rate in Scramble, TGIF2-OE, siSOX2, TGIF2-OE/siSOX2 and TGIF2-OE/Erlotinib groups of PANC-1 cells and in Scramble, siTGIF2, SOX2-OE and siTGIF2/SOX2-OE of BxPC-3 cells by MTT. Bars indicate ± S.E.*, P <0.05; **, P <0.01 compared with the control.

Techniques: In Vitro, Activation Assay, Expressing, Mutagenesis, Over Expression, Concentration Assay, Control

TGIF2 is a transactivation factor of SOX2 and interacts with Smad2 to co-regulate SOX2. A. The mRNA level of TGIF2 and SOX2 in TGIF2 overexpressing PANC-1 and TGIF2 silencing BxPC-3 cells, respectively. B. The binding site of TGIF2 in its zinc fingers domain was obtained from the JASPAR database. C. The predicted potential binding site of TGIF2 to SOX2 promoter, as well as wild-type/mutant SOX2 promoter plasmids (SOX2-WT or SOX2-Mut) designed accordingly. D. Chip assays in PANC-1 and BxPC-3 cells. E. Luciferase assay in 293 T cells co-transfected with SOX2-WT or SOX2-Mut promoter plasmid and TGIF2 overexpression plasmid. F. The protein interaction network of TGIF2 via String database. G. Co-IP was performed in PANC-1 and BxPC-3 cells. H and I. The protein and mRNA level of Smad2 and SOX2 in Smad2 silencing BxPC-3 cells. J. The binding site of Smad2 in its zinc fingers domain was obtained from the JASPAR database. K. The predicted potential binding site of Smad2 to SOX2 promoter, as well as wild-type/mutant SOX2 promoter plasmids (SOX2-WT or SOX2-Mut2) designed accordingly. L. Chip assays in BxPC-3 cells. M. Luciferase assay in 293 T cells co-transfected with SOX2-WT or SOX2-Mut2 promoter plasmid and Smad2 overexpression plasmid (or empty vector scramble). N. The protein level of Smad2 and SOX2 in Scramble, TGIF2-OE, si2-Smad2 and TGIF2-OE/si2-Smad2 groups in PANC-1 cells. Bars indicate ± S.E.*, P <0.05; **, P <0.01 in contrast with the control.

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: TGIF2 is a transactivation factor of SOX2 and interacts with Smad2 to co-regulate SOX2. A. The mRNA level of TGIF2 and SOX2 in TGIF2 overexpressing PANC-1 and TGIF2 silencing BxPC-3 cells, respectively. B. The binding site of TGIF2 in its zinc fingers domain was obtained from the JASPAR database. C. The predicted potential binding site of TGIF2 to SOX2 promoter, as well as wild-type/mutant SOX2 promoter plasmids (SOX2-WT or SOX2-Mut) designed accordingly. D. Chip assays in PANC-1 and BxPC-3 cells. E. Luciferase assay in 293 T cells co-transfected with SOX2-WT or SOX2-Mut promoter plasmid and TGIF2 overexpression plasmid. F. The protein interaction network of TGIF2 via String database. G. Co-IP was performed in PANC-1 and BxPC-3 cells. H and I. The protein and mRNA level of Smad2 and SOX2 in Smad2 silencing BxPC-3 cells. J. The binding site of Smad2 in its zinc fingers domain was obtained from the JASPAR database. K. The predicted potential binding site of Smad2 to SOX2 promoter, as well as wild-type/mutant SOX2 promoter plasmids (SOX2-WT or SOX2-Mut2) designed accordingly. L. Chip assays in BxPC-3 cells. M. Luciferase assay in 293 T cells co-transfected with SOX2-WT or SOX2-Mut2 promoter plasmid and Smad2 overexpression plasmid (or empty vector scramble). N. The protein level of Smad2 and SOX2 in Scramble, TGIF2-OE, si2-Smad2 and TGIF2-OE/si2-Smad2 groups in PANC-1 cells. Bars indicate ± S.E.*, P <0.05; **, P <0.01 in contrast with the control.

Techniques: Binding Assay, Zinc-Fingers, Mutagenesis, Luciferase, Transfection, Plasmid Preparation, Over Expression, Co-Immunoprecipitation Assay, Control

SOX2 is a transactivation factor of EGFR and Slug. A. The mRNA level of SOX2, EGFR and Slug in SOX2 overexpressing PANC-1 and SOX2 silencing BxPC-3 cells, respectively. B. The DNA binding site of SOX2 was obtained from the JASPAR database. C. The predicted potential binding site of SOX2 to Slug promoter. D and E. Chip assays in PANC-1 (D) and BxPC-3 (E) cells. F. The predicted potential binding site of SOX2 to EGFR promoter, as well as wild-type/mutant EGFR promoter plasmids designed accordingly. G. Chip assays in PANC-1 and BxPC-3 cells. H. Luciferase assay in 293 T cells co-transfected with EGFR-WT (or EGFR-Mut) promoter plasmid and SOX2 overexpression plasmid (or empty vector corresponding to scramble group). I. The roles of SOX2-OE and Erlotinib treatment to TGIF2 nuclear translocation. J. IF staining of TGIF2 and SOX2 in Scramble, SOX2-OE and SOX2-OE plus Erlotinib groups of PANC-1. Bars indicate ± S.E.*, P <0.05; **, P <0.01 in contrast with the control.

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: SOX2 is a transactivation factor of EGFR and Slug. A. The mRNA level of SOX2, EGFR and Slug in SOX2 overexpressing PANC-1 and SOX2 silencing BxPC-3 cells, respectively. B. The DNA binding site of SOX2 was obtained from the JASPAR database. C. The predicted potential binding site of SOX2 to Slug promoter. D and E. Chip assays in PANC-1 (D) and BxPC-3 (E) cells. F. The predicted potential binding site of SOX2 to EGFR promoter, as well as wild-type/mutant EGFR promoter plasmids designed accordingly. G. Chip assays in PANC-1 and BxPC-3 cells. H. Luciferase assay in 293 T cells co-transfected with EGFR-WT (or EGFR-Mut) promoter plasmid and SOX2 overexpression plasmid (or empty vector corresponding to scramble group). I. The roles of SOX2-OE and Erlotinib treatment to TGIF2 nuclear translocation. J. IF staining of TGIF2 and SOX2 in Scramble, SOX2-OE and SOX2-OE plus Erlotinib groups of PANC-1. Bars indicate ± S.E.*, P <0.05; **, P <0.01 in contrast with the control.

Techniques: Binding Assay, Mutagenesis, Luciferase, Transfection, Plasmid Preparation, Over Expression, Translocation Assay, Staining, Control

Coordination of TGIF2/SOX2 promotes subcutaneous tumor size in vivo . A. Tumor volumes in Scramble, TGIF2-OE, TGIF2-OE/shSOX2, and TGIF2-OE plus Erlotinib groups implanted with PANC-1 cells. B. Tumor growth curve in above group. C. HE staining of harvested tumor. D. The statistical data of IHC assays. E. The different expression of TGIF2, SOX2, E-cad, EGFR and Vimentin in Scramble, TGIF2-OE, and TGIF2-OE/shSOX2 groups by IHC. Bars indicate ± S.E. *, P<0.05; **, P<0.01 compared with control.

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: Coordination of TGIF2/SOX2 promotes subcutaneous tumor size in vivo . A. Tumor volumes in Scramble, TGIF2-OE, TGIF2-OE/shSOX2, and TGIF2-OE plus Erlotinib groups implanted with PANC-1 cells. B. Tumor growth curve in above group. C. HE staining of harvested tumor. D. The statistical data of IHC assays. E. The different expression of TGIF2, SOX2, E-cad, EGFR and Vimentin in Scramble, TGIF2-OE, and TGIF2-OE/shSOX2 groups by IHC. Bars indicate ± S.E. *, P<0.05; **, P<0.01 compared with control.

Techniques: In Vivo, Staining, Expressing, Control

Coordination of TGIF2/SOX2 promotes liver metastasis in vivo . A . Liver metastasis in Scramble, shTGIF2 and shTGIF2/SOX2-OE groups. B-C. The Liver body ratio and the number of liver metastases in above groups. D. The different expression of TGIF2, SOX2, E-cad, EGFR and Vimentin in Scramble, shTGIF2 and shTGIF2/SOX2-OE groups by IHC. E. The statistical data of IHC assays. Bars indicate ± S.E. *, P<0.05; **, P<0.01 compared with control.

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: Coordination of TGIF2/SOX2 promotes liver metastasis in vivo . A . Liver metastasis in Scramble, shTGIF2 and shTGIF2/SOX2-OE groups. B-C. The Liver body ratio and the number of liver metastases in above groups. D. The different expression of TGIF2, SOX2, E-cad, EGFR and Vimentin in Scramble, shTGIF2 and shTGIF2/SOX2-OE groups by IHC. E. The statistical data of IHC assays. Bars indicate ± S.E. *, P<0.05; **, P<0.01 compared with control.

Techniques: In Vivo, Expressing, Control

Smad2 cooperating with TGIF2 contributes to CSC and EMT via co-targeting SOX2. TGIF2 activates SOX2 promoter via interacting with Smad2, which stimulates EMT and EGFR/MAPK signaling by transactivating Slug and EGFR, and promoting EMT and CSCs function. Moreover, the stimulation of EGFR/MAPK signaling by SOX2 promotes TGIF2 nuclear translocation, forming a positive feedback loop.

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: Smad2 cooperating with TGIF2 contributes to CSC and EMT via co-targeting SOX2. TGIF2 activates SOX2 promoter via interacting with Smad2, which stimulates EMT and EGFR/MAPK signaling by transactivating Slug and EGFR, and promoting EMT and CSCs function. Moreover, the stimulation of EGFR/MAPK signaling by SOX2 promotes TGIF2 nuclear translocation, forming a positive feedback loop.

Techniques: Translocation Assay

The clinicopathological significance of TGIF2 and SOX2 expression in 88 cases of clinical PC samples

Journal: International Journal of Biological Sciences

Article Title: Smad2 Cooperating with TGIF2 Contributes to EMT and Cancer Stem Cells Properties in Pancreatic Cancer via Co-Targeting SOX2

doi: 10.7150/ijbs.102381

Figure Lengend Snippet: The clinicopathological significance of TGIF2 and SOX2 expression in 88 cases of clinical PC samples

Techniques: Expressing

a) Representative images of western blot analysis (biological n=3) of stemness-associated TFs SOX2, NANOG, OCT4, KLF4 and c-MYC and p53 pathway proteins, p53 and MDM2, in a panel of established and patient-derived OS, RMS and ES cell lines. Densitometric analysis is provided in Fig. S1. b) Heat maps (top) of the mean protein expression (n=3) of stemness-related TFs, p53 and MDM2. Cell lines of each sarcoma subgroup are aligned according to the calculated SI (middle). The scheme (bottom) illustrates the tumorigenicity of SI high and SI low cell lines assayed in NSG mice (n=3). c) Survival of xenograft mouse models (n=3 mice per cell line) reflecting tumor-initiating capacity and xenograft growth rates of the sarcoma cell lines tested. d) A significant positive correlation between the expression of SOX2, OCT4 and NANOG TFs and number of tumors formed by sarcoma cell lines in mice. e) Correlation between SI values and p53 protein level in individual cell lines relative to the mean expression of each sarcoma subtype. Note that all tumorigenic SI high models exhibit deregulated p53 expression and fit within the upper or lower quartiles (indicated by dotted lines). f) p53 levels in SI high models are significantly different compared to the rest of the sarcoma cell lines. Data are presented as mean ± SD. Statistical significance was determined by one-tailed Welch’s t-test (f) and by Spearman correlation coefficient (d) , *p<0.05, **p<0.01, ***p<0.001.

Journal: bioRxiv

Article Title: Dysregulation of the p53 pathway provides a therapeutic target in aggressive pediatric sarcomas with stem-like traits

doi: 10.1101/2024.01.17.576012

Figure Lengend Snippet: a) Representative images of western blot analysis (biological n=3) of stemness-associated TFs SOX2, NANOG, OCT4, KLF4 and c-MYC and p53 pathway proteins, p53 and MDM2, in a panel of established and patient-derived OS, RMS and ES cell lines. Densitometric analysis is provided in Fig. S1. b) Heat maps (top) of the mean protein expression (n=3) of stemness-related TFs, p53 and MDM2. Cell lines of each sarcoma subgroup are aligned according to the calculated SI (middle). The scheme (bottom) illustrates the tumorigenicity of SI high and SI low cell lines assayed in NSG mice (n=3). c) Survival of xenograft mouse models (n=3 mice per cell line) reflecting tumor-initiating capacity and xenograft growth rates of the sarcoma cell lines tested. d) A significant positive correlation between the expression of SOX2, OCT4 and NANOG TFs and number of tumors formed by sarcoma cell lines in mice. e) Correlation between SI values and p53 protein level in individual cell lines relative to the mean expression of each sarcoma subtype. Note that all tumorigenic SI high models exhibit deregulated p53 expression and fit within the upper or lower quartiles (indicated by dotted lines). f) p53 levels in SI high models are significantly different compared to the rest of the sarcoma cell lines. Data are presented as mean ± SD. Statistical significance was determined by one-tailed Welch’s t-test (f) and by Spearman correlation coefficient (d) , *p<0.05, **p<0.01, ***p<0.001.

Article Snippet: shRNA lentiviral particles were utilized to knockdown expression of SOX2 (#sc-38408-V, SCBT).

Techniques: Western Blot, Derivative Assay, Expressing, One-tailed Test

a) An overview of the in-house pipeline for TMA assembly followed by IHC staining and machine learning-assisted image analysis of the whole-slide scanned TMA sections. b, c) Staining intensity of p53 and stemness-related TFs assessed by computational analysis in QuPath software ( b ) or manual readout by experienced pathologist ( c ). Data shown as mean ± SD, biological n=3. d) Representative images of IHC detection of SOX2, KLF4 and p53 in xenograft tumors formed by the indicated cell lines or in positive control tissues (SOX2, fetal lungs; KLF4, seminoma; p53, tonsilla).

Journal: bioRxiv

Article Title: Dysregulation of the p53 pathway provides a therapeutic target in aggressive pediatric sarcomas with stem-like traits

doi: 10.1101/2024.01.17.576012

Figure Lengend Snippet: a) An overview of the in-house pipeline for TMA assembly followed by IHC staining and machine learning-assisted image analysis of the whole-slide scanned TMA sections. b, c) Staining intensity of p53 and stemness-related TFs assessed by computational analysis in QuPath software ( b ) or manual readout by experienced pathologist ( c ). Data shown as mean ± SD, biological n=3. d) Representative images of IHC detection of SOX2, KLF4 and p53 in xenograft tumors formed by the indicated cell lines or in positive control tissues (SOX2, fetal lungs; KLF4, seminoma; p53, tonsilla).

Article Snippet: shRNA lentiviral particles were utilized to knockdown expression of SOX2 (#sc-38408-V, SCBT).

Techniques: Immunohistochemistry, Staining, Software, Positive Control

a) Representative western blot images (right) and densitometric analysis (left) of stemness-associated TFs, p53 and MDM2 in mut-p53 MNNG/HOS and wt-p53 ESFT-15 clones with shRNA-mediated knockdown of SOX2 (shSOX2) compared with their scramble shRNA controls (shCtrl). Data presented as mean ± SD, biological n=3–4. Densitometric analysis of OCT4, c-MYC, and MDM2 proteins is provided in Fig. S10a. b) qPCR analysis of selected stemness-associated TFs in MNNG/HOS and ESFT-15 shSOX2 clones. Data are presented as mean ± SD, biological n=3, technical n=3. Analysis of remaining genes is provided in Fig. S10b. c) Sphere formation assay evaluating stem-like phenotype of MNNG/HOS and ESFT-15 sarcoma cells after SOX2 knockdown. Stem cell frequencies and probability were computed using ELDA software . Data are shown as mean ± 95% confidence interval, biological n=3–4, technical n=5. d) Representative images of sarcospheres formed by shCtrl and shSOX2 clones of MNNG/HOS and ESFT-15 cell lines. All experiments were performed using single cell-derived clones (indicated by numbers). Statistical significance was determined by one-way ANOVA with Welch’s correction followed by post-hoc Dunnett’s test ( a, b ) or Chi-square pairwise test ( c ), *p<0.05, **p<0.01, ***p<0.001.

Journal: bioRxiv

Article Title: Dysregulation of the p53 pathway provides a therapeutic target in aggressive pediatric sarcomas with stem-like traits

doi: 10.1101/2024.01.17.576012

Figure Lengend Snippet: a) Representative western blot images (right) and densitometric analysis (left) of stemness-associated TFs, p53 and MDM2 in mut-p53 MNNG/HOS and wt-p53 ESFT-15 clones with shRNA-mediated knockdown of SOX2 (shSOX2) compared with their scramble shRNA controls (shCtrl). Data presented as mean ± SD, biological n=3–4. Densitometric analysis of OCT4, c-MYC, and MDM2 proteins is provided in Fig. S10a. b) qPCR analysis of selected stemness-associated TFs in MNNG/HOS and ESFT-15 shSOX2 clones. Data are presented as mean ± SD, biological n=3, technical n=3. Analysis of remaining genes is provided in Fig. S10b. c) Sphere formation assay evaluating stem-like phenotype of MNNG/HOS and ESFT-15 sarcoma cells after SOX2 knockdown. Stem cell frequencies and probability were computed using ELDA software . Data are shown as mean ± 95% confidence interval, biological n=3–4, technical n=5. d) Representative images of sarcospheres formed by shCtrl and shSOX2 clones of MNNG/HOS and ESFT-15 cell lines. All experiments were performed using single cell-derived clones (indicated by numbers). Statistical significance was determined by one-way ANOVA with Welch’s correction followed by post-hoc Dunnett’s test ( a, b ) or Chi-square pairwise test ( c ), *p<0.05, **p<0.01, ***p<0.001.

Article Snippet: shRNA lentiviral particles were utilized to knockdown expression of SOX2 (#sc-38408-V, SCBT).

Techniques: Western Blot, Clone Assay, shRNA, Knockdown, Tube Formation Assay, Software, Derivative Assay

a) IHC analysis of SOX2 and KLF4 expression in OS, RMS and ES biopsies. b) Expression of KLF4 and SOX2 in p53-positive and p53-negative OS and ES tissues, respectively. Note that in ES, SOX2 was detected only in p53-positive biopsies. c) Representative images of SOX2 and p53 IHC analysis in ES tissue. d) Frequency of initial metastases in OS patients with KLF4- positive and KLF4-negative tumors. e) Kaplan-Meier analysis of OS patients stratified by KLF4 and p53 protein expression. f) Frequency of initial metastases in ES patients with SOX2 high and SOX2 low tumors. g) Kaplan-Meier analysis of ES patients stratified by SOX2 protein expression (cut-off for SOX2 low histoscore value was determined as ≤ 45). h) Frequency of initial metastases in pediatric sarcoma patients with p53-positive and p53-negative tumors, showing that p53 expression is associated with early metastatic disease. i) Kaplan-Meier analysis of sarcoma patients stratified by p53 protein expression and presence of initial metastases. M0, no metastatic events; M1, presence of initial metastases. Statistical significance was determined by Welch’s t-test ( a, b ), Chi-square test ( d, f, h ) and Mantel-Cox test ( e, g, i ), *p<0.05, **p<0.01, ***p<0.001.

Journal: bioRxiv

Article Title: Dysregulation of the p53 pathway provides a therapeutic target in aggressive pediatric sarcomas with stem-like traits

doi: 10.1101/2024.01.17.576012

Figure Lengend Snippet: a) IHC analysis of SOX2 and KLF4 expression in OS, RMS and ES biopsies. b) Expression of KLF4 and SOX2 in p53-positive and p53-negative OS and ES tissues, respectively. Note that in ES, SOX2 was detected only in p53-positive biopsies. c) Representative images of SOX2 and p53 IHC analysis in ES tissue. d) Frequency of initial metastases in OS patients with KLF4- positive and KLF4-negative tumors. e) Kaplan-Meier analysis of OS patients stratified by KLF4 and p53 protein expression. f) Frequency of initial metastases in ES patients with SOX2 high and SOX2 low tumors. g) Kaplan-Meier analysis of ES patients stratified by SOX2 protein expression (cut-off for SOX2 low histoscore value was determined as ≤ 45). h) Frequency of initial metastases in pediatric sarcoma patients with p53-positive and p53-negative tumors, showing that p53 expression is associated with early metastatic disease. i) Kaplan-Meier analysis of sarcoma patients stratified by p53 protein expression and presence of initial metastases. M0, no metastatic events; M1, presence of initial metastases. Statistical significance was determined by Welch’s t-test ( a, b ), Chi-square test ( d, f, h ) and Mantel-Cox test ( e, g, i ), *p<0.05, **p<0.01, ***p<0.001.

Article Snippet: shRNA lentiviral particles were utilized to knockdown expression of SOX2 (#sc-38408-V, SCBT).

Techniques: Expressing

Review

sox2 sirna human (Santa Cruz Biotechnology)

Structured Review

Images

1) Product Images from "Nestin and SOX2 Maintain self-renewal Abilities of Different Pancreatic Cancer Stem Cell Populations"

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