Journal: Oncotarget

Article Title: MEK inhibition enhances efficacy of bacillus Calmette-Guérin on bladder cancer cells by reducing release of Toll-like receptor 2-activated antimicrobial peptides

doi: 10.18632/oncotarget.18230

Figure Lengend Snippet: (A) Western blotting analyses demonstrating the reduction of Toll-like Receptor 2 (TLR2) or TLR4 protein expression in T24 cells transfected with two shRNA-expressing plasmids targeting TLR2 or TLR4 sequences (shTLR2#1, shTLR2#2, shTLR4#1 and shTLR4#2, respectively; upper panels). Non-specific scrambled shRNA was used as control. shRNA TLR2 or TLR4 knockdown cells were selected with puromycin, and infected with BCG (10 or 30 MOI for 48 h; lower panels). Phospho ERK expression was detected by Western blotting. (B) Stable clones of TLR2- or TLR4-knockdown T24 cells were treated with BCG (10 MOI for 8 h) and analyzed for expression of phosphorylated c-Jun. Phospho-Jun/total Jun expression ratios were calculated by densitometric analysis, and indicated under each lane. Expression ratios were normalized to the untreated group. (C) StableshTLR2 or shTLR4 T24 bladder cancer cells were infected with BCG (10 MOI for 8 h), followed by ELISA of antimicrobial peptides (HBD-2, HBD-3, and CAMP) in the culture supernatant. Data are mean ± SD (n=3 per group). * P <0.05 and ** P <0.01 Student's T-test. (D) ChIP assays using anti-c-Jun antibody to detect physical interactions between c-Jun and HBD2, HBD-3 or CAMP. TLR2-or TLR4-knockdown T24 cells were infected with BCG (10 MOI for 8 h) and cross-linked with 10% formaldehyde. Expressions of AMPs were calculated as the ratio of c-Jun to Input DNA expression using densitometric analysis. All expression ratios were normalized to the untreated group.

Article Snippet: To generate stable knockdown cell lines, plasmid TLR2 and TLR4 short-hairpin RNA (shRNA) constructs and a non-specific shRNA control were purchased from Qiagen (CA, USA).

Techniques: Western Blot, Expressing, Transfection, shRNA, Control, Knockdown, Infection, Clone Assay, Enzyme-linked Immunosorbent Assay

Journal: Cell Death Discovery

Article Title: Matrine induces RIP3-dependent necroptosis in cholangiocarcinoma cells

doi: 10.1038/cddiscovery.2016.96

Figure Lengend Snippet: RIP3 was required for matrine to induce necroptosis in CCA cells. ( a and b ) Endogenous RIP3 expression levels in several tumor cell lines were detected by western blot ( a ) and real-time PCR ( b ). ( c and d ) RIP3 knockdown efficiency in Mz-ChA-1 (Left) and QBC939 (Right) cells was determined by western blot ( c ) and real-time PCR ( d ). * P <0.05, ** P <0.01 and *** P <0.001 versus control (assessed by Student’s t -test). ( e ) Mz-ChA-1 and QBC939 cells expressing control or RIP3 shRNA were pre-treated with Nec-1 (20 μ M) or z-VAD-fmk (20 μ M) for 2 h, and then treated with matrine (1.5 mg/ml) or vehicle for 48 h. After that, the percentage of cell death was determined by PI staining and flow cytometry. Results were presented as the mean±S.D. from three independent experiments. Significant differences were indicated as * P <0.05, ** P <0.01 and *** P <0.001 (assessed by Student’s t -test). ( f ) Matrine increased RIP3 expression levels in Mz-ChA-1 and QBC939 cells. Cells were treated with matrine (1.5 mg/ml) for 0, 3, 6, 9 and 12 h, then lysed and subjected to western blot analysis with anti-RIP3 antibody. β -actin was used as an internal control.

Article Snippet: Human RIP3 shRNAs and non-targeting control shRNA were purchased from Shanghai Genechem.

Techniques: Expressing, Western Blot, Real-time Polymerase Chain Reaction, Knockdown, Control, shRNA, Staining, Flow Cytometry

Journal: BMC Cancer

Article Title: Troglitazone suppresses telomerase activity independently of PPARγ in estrogen-receptor negative breast cancer cells

doi: 10.1186/1471-2407-10-390

Figure Lengend Snippet: The suppressive role of troglitazone on telomerase is independent from PPARγ . A) MDA-MB-231 cells were exposed to either 10 μM GW9662 or 100 μM BADGE for 24 hours. Cells then were treated with 20 μM troglitazone in the presence of GW9662 or BADGE for another 24 hours. At the end of the incubation time, the expression level of hTERT was determined by real time RT-PCR. Values are expressed as the percentage of vehicle-treated controls (DMSO) in the respective treatment condition. Results shown are as mean ± SD and are representative of three independent experiments. B) Utilizing shRNA interference, the expression of PPARγ was inhibited with four different shRNA oligos (71, 72, 73, and 74) in the MDA-MB-231 cell line. To assess the specificity of shRNA oligos against PPARγ , MDA-MB-231 cells were transfected with scrambled oligo as a control. The mRNA level of PPARγ was examined by real-time RT-PCR. WT, non-infected cells; SCR, scrambled oligo; 71-74 shRNA oligos. C) The TRAP assay was used to examine the activity of telomerase in MDA-MB-231 cells in the absence of PPARγ (Oligo 71, 72, 73, 74) compared to non-infected MDA-MB-231 cells (WT) and cells transfected with a scrambled oligo which acted as non-silencing control shRNA sequence (SCR). (500 and 250 ng of cell lysate, respectively. D) MDA-MB-231 cells carrying silenced PPARγ by shRNA were treated with 20 μM troglitazone or the equal volume of DMSO for 24 hours and telomerase activity was measured using the TRAP assay (500 and 250 ng of cell lysate, respectively). C and D) I.C., the internal PCR amplification control. CHAPS, lysis buffer only as a negative control. HeLa, 500 cell equivalent lysate as a positive control. Result shown is representative of two independent experiments.

Article Snippet: An adopted Qiagen non-silencing control shRNA sequence (TTCTCCGAACGTGTCACGT) that was not complementary to any human gene was used as a control shRNA (generous gift from Dr. M.S.

Techniques: Incubation, Expressing, Quantitative RT-PCR, shRNA, Transfection, Control, Infection, TRAP Assay, Activity Assay, Sequencing, Amplification, Lysis, Negative Control, Positive Control

Journal: Molecular Medicine Reports

Article Title: lncRNA FEZF1-AS1 promotes migration, invasion and epithelial-mesenchymal transition of retinoblastoma cells by targeting miR-1236-3p

doi: 10.3892/mmr.2020.11478

Figure Lengend Snippet: Oligonucleotide sequences used for the transfection experiments.

Article Snippet: Synthetic sequences of short hairpin RNA (shRNA) targeting FEZF1-AS1 (shRNA-FEZF1-AS1; Shanghai GenePharma Co., Ltd.) and non-targeting shRNA (shRNA-NC) were inserted into pGPU6/Neo vector (Shanghai GenePharma Co., Ltd.).

Techniques: Transfection, Sequencing, shRNA

Journal: Molecular Medicine Reports

Article Title: lncRNA FEZF1-AS1 promotes migration, invasion and epithelial-mesenchymal transition of retinoblastoma cells by targeting miR-1236-3p

doi: 10.3892/mmr.2020.11478

Figure Lengend Snippet: Overexpression of FEZF1-AS1 in Rb cells. (A) Expression levels of FEZF1-AS1 were analyzed in four Rb cell lines and ARPE-19 cells (control) using RT-qPCR. **P<0.01, ***P<0.001 vs. control. (B) RT-qPCR analysis of the transfection efficiency of shRNA-FEZF1-AS1. ***P<0.001 vs. shRNA-NC group. All data are expressed as the mean ± SEM. Rb, retinoblastoma; FEZF1-AS1, FEZ family zinc finger 1 antisense RNA 1; RT-qPCR, reverse transcription- quantitative PCR; shRNA, short hairpin RNA; NC, negative control.

Article Snippet: Synthetic sequences of short hairpin RNA (shRNA) targeting FEZF1-AS1 (shRNA-FEZF1-AS1; Shanghai GenePharma Co., Ltd.) and non-targeting shRNA (shRNA-NC) were inserted into pGPU6/Neo vector (Shanghai GenePharma Co., Ltd.).

Techniques: Over Expression, Expressing, Quantitative RT-PCR, Transfection, shRNA, Real-time Polymerase Chain Reaction, Negative Control

Journal: Molecular Medicine Reports

Article Title: lncRNA FEZF1-AS1 promotes migration, invasion and epithelial-mesenchymal transition of retinoblastoma cells by targeting miR-1236-3p

doi: 10.3892/mmr.2020.11478

Figure Lengend Snippet: Silencing FEZF1-AS1 inhibits cell viability, migration and invasion. (A) Cell viability was determined in Y79 cells transfected with shRNA-NC or shRNA-FEZF1-AS1 using a Cell Counting Kit-8 assay. (B) Cell migratory rate was determined in Y79 cells transfected with shRNA-NC or shRNA-FEZF1-AS1 using a wound healing assay. Magnification, ×100. (C) Cell invasive rate was determined in Y79 cells transfected with shRNA-NC or shRNA-FEZF1-AS1 using a Transwell Matrigel invasion assay. Magnification ×100. All data are expressed as the mean ± SEM. ***P<0.001 vs. shRNA-NC group. FEZF1-AS1, FEZ family zinc finger 1 antisense RNA 1; shRNA, short hairpin RNA; NC, negative control.

Article Snippet: Synthetic sequences of short hairpin RNA (shRNA) targeting FEZF1-AS1 (shRNA-FEZF1-AS1; Shanghai GenePharma Co., Ltd.) and non-targeting shRNA (shRNA-NC) were inserted into pGPU6/Neo vector (Shanghai GenePharma Co., Ltd.).

Techniques: Migration, Transfection, shRNA, Cell Counting, Wound Healing Assay, Invasion Assay, Negative Control

Journal: Molecular Medicine Reports

Article Title: lncRNA FEZF1-AS1 promotes migration, invasion and epithelial-mesenchymal transition of retinoblastoma cells by targeting miR-1236-3p

doi: 10.3892/mmr.2020.11478

Figure Lengend Snippet: Epithelial-mesenchymal transition of retinoblastoma cells is suppressed by shRNA-FEZF1-AS1. Western blotting was used to analyze the protein expression levels of (A) Vimentin, Snail, Slug and β-catenin, (B) N-cadherin, E-cadherin, Claudin-1 and (C) MMP2 and MMP9 in Y79 cells transfected with shRNA-NC or shRNA-FEZF1-AS1. All data are expressed as the mean ± SEM. **P<0.01, ***P<0.001 vs. shRNA-NC group. FEZF1-AS1, FEZ family zinc finger 1 antisense RNA 1; shRNA, short hairpin RNA; NC, negative control; MMP, matrix metalloproteinase.

Article Snippet: Synthetic sequences of short hairpin RNA (shRNA) targeting FEZF1-AS1 (shRNA-FEZF1-AS1; Shanghai GenePharma Co., Ltd.) and non-targeting shRNA (shRNA-NC) were inserted into pGPU6/Neo vector (Shanghai GenePharma Co., Ltd.).

Techniques: shRNA, Western Blot, Expressing, Transfection, Negative Control

Journal: Molecular Medicine Reports

Article Title: lncRNA FEZF1-AS1 promotes migration, invasion and epithelial-mesenchymal transition of retinoblastoma cells by targeting miR-1236-3p

doi: 10.3892/mmr.2020.11478

Figure Lengend Snippet: miR-1236-3p is a direct target of FEZF1-AS1 in retinoblastoma cells. (A) Binding sites between FEZF1-AS1 and miR-1236-3p were predicted using LncBase v.2 software. (B) RNA immunoprecipitation assay was performed to analyze the interaction between miR-1236-3p and FEZF1-AS1 in Y79 cells co-transfected with miR-1236-3p mimic or miR-NC mimic and FEZF1-AS1-WT or FEZF1-AS1-MUT. ***P<0.001 vs. IgG group. (C) Relative luciferase activity was determined using a dual-luciferase reporter assay in cells co-transfected with miR-1236-3p mimic or miR-NC mimic and FEZF1-AS1-WT or FEZF1-AS1-MUT. ***P<0.001 vs. miR-NC mimic group. (D) Expression levels of miR-1236-3p were detected in Y79 cells transfected with shRNA-NC or shRNA-FEZF1-AS1 using RT-qPCR. ***P<0.001 vs. shRNA-NC group. (E) Expression levels of FEZF1-AS1 were analyzed in Y79 cells transfected with miR-NC mimic or miR-1236-3p mimic by RT-qPCR. **P<0.01 vs. miR-NC mimic group. All data are expressed as the mean ± SEM. FEZF1-AS1, FEZ family zinc finger 1 antisense RNA 1; shRNA, short hairpin RNA; NC, negative control; miR, microRNA; WT, wild-type; MUT, mutant; RT-qPCR, reverse transcription-quantitative PCR.

Article Snippet: Synthetic sequences of short hairpin RNA (shRNA) targeting FEZF1-AS1 (shRNA-FEZF1-AS1; Shanghai GenePharma Co., Ltd.) and non-targeting shRNA (shRNA-NC) were inserted into pGPU6/Neo vector (Shanghai GenePharma Co., Ltd.).

Techniques: Binding Assay, Software, Immunoprecipitation, Transfection, Luciferase, Activity Assay, Reporter Assay, Expressing, shRNA, Quantitative RT-PCR, Negative Control, Mutagenesis, Real-time Polymerase Chain Reaction

Journal: Molecular Medicine Reports

Article Title: lncRNA FEZF1-AS1 promotes migration, invasion and epithelial-mesenchymal transition of retinoblastoma cells by targeting miR-1236-3p

doi: 10.3892/mmr.2020.11478

Figure Lengend Snippet: miR-1236-3p inhibitor reverses shRNA-FEZF1-AS1-induced suppression over cell viability, migration and invasion. (A) Cell viability was determined in Y79 cells transfected with shRNA-NC or shRNA-FEZF1-AS1 with or without miR-1236-3p inhibitor or miR-NC inhibitor using a Cell-Counting Kit-8 assay. (B and D) Migratory rates were determined in Y79 cells transfected with shRNA-NC or shRNA-FEZF1-AS1 with or without miR-1236-3p inhibitor or miR-NC inhibitor using wound healing assay. Magnification, ×100. (C and E) Invasive rates were determined in Y79 cells transfected with shRNA-NC or shRNA-FEZF1-AS1 with or without miR-1236-3p inhibitor or miR-NC inhibitor using Transwell Matrigel assay. Magnification, ×100. All data are expressed as the mean ± SEM. ***P<0.001 vs. shRNA-NC group; ## P<0.01 vs. shRNA-FEZF1-AS1 + miR-NC inhibitor group. FEZF1-AS1, FEZ family zinc finger 1 antisense RNA 1; shRNA, short hairpin RNA; NC, negative control; miR, microRNA.

Article Snippet: Synthetic sequences of short hairpin RNA (shRNA) targeting FEZF1-AS1 (shRNA-FEZF1-AS1; Shanghai GenePharma Co., Ltd.) and non-targeting shRNA (shRNA-NC) were inserted into pGPU6/Neo vector (Shanghai GenePharma Co., Ltd.).

Techniques: shRNA, Migration, Transfection, Cell Counting, Wound Healing Assay, Matrigel Assay, Negative Control

Journal: Molecular Medicine Reports

Article Title: lncRNA FEZF1-AS1 promotes migration, invasion and epithelial-mesenchymal transition of retinoblastoma cells by targeting miR-1236-3p

doi: 10.3892/mmr.2020.11478

Figure Lengend Snippet: Continued. Inhibition of miR-1236-3p reverses the effects of shRNA-FEZF1-AS1 on epithelial-mesenchymal transition. (A) Western blotting was used to analyze the protein expression levels of (A) Vimentin, Snail, Slug and β-catenin, (B) N-cadherin, E-cadherin and Claudin-1, and (C) MMP2 and MMP9 in Y79 cells transfected with shRNA-NC or shRNA-FEZF1-AS1 with or without miR-1236-3p inhibitor or miR-NC inhibitor. All data are expressed as the mean ± SEM. ***P<0.001 vs. shRNA-NC group; # P<0.05, ## P<0.01, ### P<0.001 vs. shRNA-FEZF1-AS1 + miR-NC inhibitor group. FEZF1-AS1, FEZ family zinc finger 1 antisense RNA 1; shRNA, short hairpin RNA; NC, negative control; miR, microRNA; MMP, matrix metalloproteinase.

Article Snippet: Synthetic sequences of short hairpin RNA (shRNA) targeting FEZF1-AS1 (shRNA-FEZF1-AS1; Shanghai GenePharma Co., Ltd.) and non-targeting shRNA (shRNA-NC) were inserted into pGPU6/Neo vector (Shanghai GenePharma Co., Ltd.).

Techniques: Inhibition, shRNA, Western Blot, Expressing, Transfection, Negative Control

Journal: BMC Cancer

Article Title: Interaction between DNMT3B and MYH11 via hypermethylation regulates gastric cancer progression

doi: 10.1186/s12885-021-08653-3

Figure Lengend Snippet: Primer used for RT-qPCR

Article Snippet: The overexpressed (oe) DNA plasmids oe-MYH11, oe-TNFRSF14, oe-DNMT3B and control oe-negative control (NC) used for cell transfection were from VectorBuilder (Guangzhou, Guangdong, China).

Techniques:

Journal: BMC Cancer

Article Title: Interaction between DNMT3B and MYH11 via hypermethylation regulates gastric cancer progression

doi: 10.1186/s12885-021-08653-3

Figure Lengend Snippet: DNMT3B upregulation is responsible for the hypermethylation of the MYH11 promoter. A , the expression of DNMT3A and DNMT3B in GC was queried in StarBase Pan-cancer platform; B , the enrichment ability of DNMT3A and DNMT3B on MYH11 promoter examined by ChIP-qPCR; C , DNMT3B mRNA expression in GC tumor tissues and their adjacent tissues by RT-qPCR; D , correlation of DNMT3B expression with MYH11 promoter methylation levels in tumor tissues analyzed by Pearson’s correlation analysis (r = 0.623, p < 0.001); E , correlation of DNMT3B expression with MYH11 expression in tumor tissues (r = − 0.609, p < 0.001); F , transfection efficiency of oe-DNMT3B in GC cells by RT-qPCR; G , the effects of DNMT3B overexpression on the methylation level of MYH11 promoter examined by qMSP; H , effects of DNMT3B overexpression on MYH11 expression by RT-qPCR. Each assay was performed at least three times. Statistical significance was analyzed by paired t test (panel C) or two-way ANOVA (panels B, F, G and H) and Tukey’s multiple range tests

Article Snippet: The overexpressed (oe) DNA plasmids oe-MYH11, oe-TNFRSF14, oe-DNMT3B and control oe-negative control (NC) used for cell transfection were from VectorBuilder (Guangzhou, Guangdong, China).

Techniques: Expressing, Quantitative RT-PCR, Methylation, Transfection, Over Expression

Journal: BMC Cancer

Article Title: Interaction between DNMT3B and MYH11 via hypermethylation regulates gastric cancer progression

doi: 10.1186/s12885-021-08653-3

Figure Lengend Snippet: Mechanism diagram. Overexpression of DNMT3B in GC inhibited MYH11 expression by promoting methylation of the MYH11 promoter, thereby attenuating the repressive effect of MYH11 on TNFRSF14 transcriptional activity and promoting GC progression

Article Snippet: The overexpressed (oe) DNA plasmids oe-MYH11, oe-TNFRSF14, oe-DNMT3B and control oe-negative control (NC) used for cell transfection were from VectorBuilder (Guangzhou, Guangdong, China).

Techniques: Over Expression, Expressing, Methylation, Activity Assay

Journal: Cell Biology and Toxicology

Article Title: EIF4A3-mediated oncogenic circRNA hsa_circ_0001165 advances esophageal squamous cell carcinoma progression through the miR-381-3p/TNS3 pathway

doi: 10.1007/s10565-024-09927-9

Figure Lengend Snippet: Silencing of hsa_circ_0001165 Suppresses Esophageal Cancer Cell Proliferation, Migration, and Invasion In Vitro. ( A ) PCR analysis was conducted to measure the expression levels of hsa_circ_0001165 in KYSE30 and KYSE150 cells following treatment with shRNA (sh-circ_0001165). ( B ) The CCK-8 assay was performed to evaluate the viability of KYSE30 and KYSE150 cells. ( C ) An EdU assay was carried out to assess the proliferative capacity of KYSE30 and KYSE150 cells. ( D ) A colony formation assay was executed to analyze the proliferation potential of KYSE30 and KYSE150 cells. ( E ) A wound healing assay was utilized to determine the migratory ability of esophageal cancer cells. ( F ) A Transwell assay was employed to assess the migratory and invasive capabilities of esophageal cancer cells. * P < 0.05, ** P < 0.01, *** P < 0.001, as determined by a Students t-test

Article Snippet: The shRNA targeting hsa_circ_0001165 was suppressed via lentiviral transduction, with a non-targeting shRNA as the control, both synthesized by OBiO Technology (Shanghai, China).

Techniques: Migration, In Vitro, Expressing, shRNA, CCK-8 Assay, EdU Assay, Colony Assay, Wound Healing Assay, Transwell Assay

Journal: Cell Reports Medicine

Article Title: Myeloid cells coordinately induce glioma cell-intrinsic and cell-extrinsic pathways for chemoresistance via GP130 signaling

doi: 10.1016/j.xcrm.2024.101658

Figure Lengend Snippet: Humanin-induced chemoresistance requires ATR signaling (A) hGBM1 cells were stimulated with HN or vehicle (Ctrl.), underwent transcriptomics, and differentially expressed genes (DEGs) were analyzed by bioinformatics. (B) Experiments described in (A) were repeated with hGBM-1, 2, and 3 cells providing 12 consistent DEGs, of which several components assembled in a network. (C) HUS1 was associated with outcome in human GBMs. (D) In a myeloid-free brain sample, hGBMs have a basal level of HUS1 expression, which is upregulated by interaction with hiPSC microglia in a GP130-dependent manner. (E and F) Contribution of the ATR pathway to humanin-induced GBM expansion (E) and chemoresistance (F) was demonstrated with the ATR inhibitor AZ20. (G) Western blots showing expression levels of HUS1, ATR and beta-actin (loading control) and a readout for of ATR activation (pT1989) in hGBM1 cells treated with bovine serum albumin (control), TMZ, HN, or AZ20. (H) In summary, AZ20 does not cooperate with TMZ per se, but blocks HN-induced TMZ resistance. The number of biological replicates is indicated (dots in graphs indicate data from individual experiments); all error bars are presented as mean ± SDM. Statistical significance is shown as FDR in (A), one-way ANOVA (D, E), or two-way ANOVA (F): ∗ p < 0.05; ∗∗∗ p < 0.001; ∗∗∗∗ p < 0.0001; NS, not significant.

Article Snippet: HUS1 shRNA lentiviral and non-target control constructs , BioCat , Cat#: TLHSU1400-3364-pZIP-hCMV-ZsGreen-GVO-TRI.

Techniques: Expressing, Western Blot, Control, Activation Assay

Journal: Cell Reports Medicine

Article Title: Myeloid cells coordinately induce glioma cell-intrinsic and cell-extrinsic pathways for chemoresistance via GP130 signaling

doi: 10.1016/j.xcrm.2024.101658

Figure Lengend Snippet: Humanin-induced chemoresistance can be blocked therapeutically (A) Tumor size of orthotopic HN-WT or HN-C8a tumors was compared in mice receiving TMZ or vehicle (in animals with established tumor growth, 5x per week for 2 weeks; pre-defined endpoint was at 3 weeks). (B) Orthotopic hGBM1 was infused with HN (100 nM) or vehicle (artificial cerebrospinal fluid, aCSF) and i.p. injected with bazedoxifene-A (5 injections of BZA per week; 40 mg/kg; for 2 weeks) or vehicle; brains were labeled for HUS1; HUS1 expression was quantified. (C) Mice with established, orthotopic HN-WT tumors received TMZ (50 mg/kg) and were cotreated with vehicle or BZA (as in B); after 3 weeks, tumor size was quantified (dashed line: average data from untreated WT GBMs). (D) Mice with HN-WT GBMs received TMZ and were cotreated with vehicle or BZA (as in C); GBM samples were immunostained for active caspase-3 and immunolabeling was quantified (dashed line: average data from untreated WT GBMs). (E) Intratumoral vascularization and vessel diameter were compared in HN-WT or HN-C8a tumors receiving TMZ. (F) The HN-WT GBM mouse model was i.p. injected with TMZ and cotreated either with BZA or vehicle and the extent of intratumoral vascularization was compared. The number of biological replicates is indicated (dots in graphs indicate data from individual mice); all error bars are presented as mean ± SDM. Statistical significance is shown by one-way ANOVA (A, E), two-way ANOVA (B–D), or t test (F): ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; NS, not significant. Scale bars in (B, C) indicate 1 mm; scales in (D) represent 500 (overview) or 10 μm (magnified).

Article Snippet: HUS1 shRNA lentiviral and non-target control constructs , BioCat , Cat#: TLHSU1400-3364-pZIP-hCMV-ZsGreen-GVO-TRI.

Techniques: Injection, Labeling, Expressing, Immunolabeling

Journal: Cell Reports Medicine

Article Title: Myeloid cells coordinately induce glioma cell-intrinsic and cell-extrinsic pathways for chemoresistance via GP130 signaling

doi: 10.1016/j.xcrm.2024.101658

Figure Lengend Snippet:

Article Snippet: HUS1 shRNA lentiviral and non-target control constructs , BioCat , Cat#: TLHSU1400-3364-pZIP-hCMV-ZsGreen-GVO-TRI.

Techniques: Plasmid Preparation, Recombinant, Transfection, Fluorescence, Staining, Reverse Transcription, Expressing, Liposomes, Mutagenesis, shRNA, Control, Construct, Software, Imaging, Functional Assay, Dissection, Sequencing, Real-time Polymerase Chain Reaction