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BioResource International Inc japanese escc cell lines
Japanese Escc Cell Lines, supplied by BioResource International Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/japanese+escc+cell+lines/pm22309361-43-25-39?v=BioResource+International+Inc
Average 90 stars, based on 1 article reviews

japanese escc cell lines - by Bioz Stars, 2026-07

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Fig. 1 Low pGSN level correlates with cancer progression and poor prognosis in ESCC patients. A ELISA analysis of circulating pGSN in ESCC patients (N = 172) stratified by different stages. A total of 28 normal individuals were included as a control group. B Quantitative difference of GSN expression in the GTEx (normal) and TCGA (tumor) datasets. C ELISA analysis of circulating pGSN in ESCC patients with good CCRT response (n = 64) or poor CCRT response (n = 96). D and E Kaplan–Meier plots of overall (D) and progression-free survival. (E) Survival analysis based on the circulating pGSN expression. The optimal cutoff level was set using Fisher’s exact test. F Basal levels of pGSN expression in cell lysate and CM of the resistant (R) or parental (P) cells were examined by Western blot analysis. GAPDH was used as an internal control. G MTT assay of resistant and parental ESCC cells treated with various concentrations of cisplatin for 72 h. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Journal: Journal of biomedical science

Article Title: Decreased plasma gelsolin fosters a fibrotic tumor microenvironment and promotes chemoradiotherapy resistance in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-024-01078-7

Figure Lengend Snippet: Fig. 1 Low pGSN level correlates with cancer progression and poor prognosis in ESCC patients. A ELISA analysis of circulating pGSN in ESCC patients (N = 172) stratified by different stages. A total of 28 normal individuals were included as a control group. B Quantitative difference of GSN expression in the GTEx (normal) and TCGA (tumor) datasets. C ELISA analysis of circulating pGSN in ESCC patients with good CCRT response (n = 64) or poor CCRT response (n = 96). D and E Kaplan–Meier plots of overall (D) and progression-free survival. (E) Survival analysis based on the circulating pGSN expression. The optimal cutoff level was set using Fisher’s exact test. F Basal levels of pGSN expression in cell lysate and CM of the resistant (R) or parental (P) cells were examined by Western blot analysis. GAPDH was used as an internal control. G MTT assay of resistant and parental ESCC cells treated with various concentrations of cisplatin for 72 h. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Article Snippet: Japanese ESCC cell line, KYSE510, was purchased from DSMZ-German Collection of Microorganisms and Cell Cultures (Braunschweig, Lower Saxony, Germany), where they were characterized by DNA-fingerprinting and isozyme detection.

Techniques: Enzyme-linked Immunosorbent Assay, Control, Expressing, Western Blot, MTT Assay

Fig. 3 Promoter hypermethylation results in low pGSN expression in ESCC cells. A The promoter map of GSN gene. Each bar marked on the DNA strand indicates a CpG site. Primer sets for MSP analysis are labeled as Set 1 and Set 2. B and C RT-qPCR analysis of pGSN (B) and cGSN (C) mRNA expression. β-actin was used as an internal control. D, Immunoblotting of DNMT1 and pGSN in ESCC cells treated with demethylation agents 5-aza or Nutlin-3. GAPDH was used as an internal control. E MSP results demonstrated that demethylation agents (5-aza or Nutlin-3) reduced the methylation of the GSN promoter, as evidenced by an increase in U products. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Journal: Journal of biomedical science

Article Title: Decreased plasma gelsolin fosters a fibrotic tumor microenvironment and promotes chemoradiotherapy resistance in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-024-01078-7

Figure Lengend Snippet: Fig. 3 Promoter hypermethylation results in low pGSN expression in ESCC cells. A The promoter map of GSN gene. Each bar marked on the DNA strand indicates a CpG site. Primer sets for MSP analysis are labeled as Set 1 and Set 2. B and C RT-qPCR analysis of pGSN (B) and cGSN (C) mRNA expression. β-actin was used as an internal control. D, Immunoblotting of DNMT1 and pGSN in ESCC cells treated with demethylation agents 5-aza or Nutlin-3. GAPDH was used as an internal control. E MSP results demonstrated that demethylation agents (5-aza or Nutlin-3) reduced the methylation of the GSN promoter, as evidenced by an increase in U products. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Techniques: Expressing, Labeling, Quantitative RT-PCR, Control, Western Blot, Methylation

Fig. 4 pGSN inversely correlates with the expression of DNMTs and CAF markers. A Representative IHC staining images of DNMT1, DNMT3A, DNMT3B, pGSN, TNC, αSMA, collagen 1, and integrin αvβ3 expression in early and late-stage ESCC patients. B Correlation analysis of pGSN with DNMT1 (left) and TNC (right). C Protein levels of GSN, TNC, and FAP in the ESCC proteomic mass spectrum dataset (24). D Correlation analysis of pGSN with αSMA (left) or collagen 1 (right). E Proteomics revealed that most ESCC patients show an inverse expression of pGSN with TNC (upper) or FAP (bottom)

Journal: Journal of biomedical science

Article Title: Decreased plasma gelsolin fosters a fibrotic tumor microenvironment and promotes chemoradiotherapy resistance in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-024-01078-7

Figure Lengend Snippet: Fig. 4 pGSN inversely correlates with the expression of DNMTs and CAF markers. A Representative IHC staining images of DNMT1, DNMT3A, DNMT3B, pGSN, TNC, αSMA, collagen 1, and integrin αvβ3 expression in early and late-stage ESCC patients. B Correlation analysis of pGSN with DNMT1 (left) and TNC (right). C Protein levels of GSN, TNC, and FAP in the ESCC proteomic mass spectrum dataset (24). D Correlation analysis of pGSN with αSMA (left) or collagen 1 (right). E Proteomics revealed that most ESCC patients show an inverse expression of pGSN with TNC (upper) or FAP (bottom)

Techniques: Expressing, Immunohistochemistry

Fig. 5 pGSN competes with TNC for binding to integrin αvβ3. A Schematic of cell-based IP analysis. B Western blot analysis of membrane-anchored integrin IP discovered an integrin-binding competition between pGSN and TNC in ESCC. GAPDH was used as an internal control. C Western blot analysis of CHX chase assay to investigate the protein stability of integrin αvβ3. GAPDH was used as an internal control. D Integrin downstream signaling p-FAK and p-paxillin was examined by IF staining. E Western blot analysis of TNC expression in pGSN-overexpressing cells. GAPDH was used as an internal control

Journal: Journal of biomedical science

Article Title: Decreased plasma gelsolin fosters a fibrotic tumor microenvironment and promotes chemoradiotherapy resistance in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-024-01078-7

Figure Lengend Snippet: Fig. 5 pGSN competes with TNC for binding to integrin αvβ3. A Schematic of cell-based IP analysis. B Western blot analysis of membrane-anchored integrin IP discovered an integrin-binding competition between pGSN and TNC in ESCC. GAPDH was used as an internal control. C Western blot analysis of CHX chase assay to investigate the protein stability of integrin αvβ3. GAPDH was used as an internal control. D Integrin downstream signaling p-FAK and p-paxillin was examined by IF staining. E Western blot analysis of TNC expression in pGSN-overexpressing cells. GAPDH was used as an internal control

Techniques: Binding Assay, Western Blot, Membrane, Control, Staining, Expressing

Fig. 8 Schematic model of pGSN deficient fostering a fibrotic tumor environment of ESCC. In early-stage ESCC patients, extracellular pGSN competes with oncogenic TNC for binding to integrin αvβ3, reducing its stability and suppressing oncogenic signaling. During ESCC tumor progression, GSN gene methylation causes decreased secretion of pGSN, leading to integrin αvβ3 dysregulation, oncogenic TNC activation, and CAF formation

Journal: Journal of biomedical science

Article Title: Decreased plasma gelsolin fosters a fibrotic tumor microenvironment and promotes chemoradiotherapy resistance in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-024-01078-7

Figure Lengend Snippet: Fig. 8 Schematic model of pGSN deficient fostering a fibrotic tumor environment of ESCC. In early-stage ESCC patients, extracellular pGSN competes with oncogenic TNC for binding to integrin αvβ3, reducing its stability and suppressing oncogenic signaling. During ESCC tumor progression, GSN gene methylation causes decreased secretion of pGSN, leading to integrin αvβ3 dysregulation, oncogenic TNC activation, and CAF formation

Techniques: Binding Assay, Methylation, Activation Assay

Fig. 2 SOX17 functions as a transcriptional repressor of NRF2. A Schematic of reporter plasmid construct used in luciferase reporter assay. The NFE2L2 promoter (− 2000 ~ + 10 bp) containing seven SOX17 binding sites was sub-cloned into the pGL4 basic vector. B Schematic of the hypothesis that SOX17-mediated transcriptional repression on NRF2 model. SRY sites: SOX17 binding residues. C Dual luciferase promoter reporter assay was performed to examine the effects of SOX17 wild type (SOX17-WT) or HMG box deletion (SOX17-ΔHMG) overexpression on promoter activity of NFE2L2 in ESCC cells. D Promoter map for NFE2L2 gene. Regions examined with ChIP assay are marked by red circle-backslash symbol. E ChIP-qPCR assay was performed to measure SOX17 binding ability to the promoter region of NFE2L2 in ESCC cells. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Journal: Journal of biomedical science

Article Title: Dysregulation of SOX17/NRF2 axis confers chemoradiotherapy resistance and emerges as a novel therapeutic target in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-022-00873-4

Figure Lengend Snippet: Fig. 2 SOX17 functions as a transcriptional repressor of NRF2. A Schematic of reporter plasmid construct used in luciferase reporter assay. The NFE2L2 promoter (− 2000 ~ + 10 bp) containing seven SOX17 binding sites was sub-cloned into the pGL4 basic vector. B Schematic of the hypothesis that SOX17-mediated transcriptional repression on NRF2 model. SRY sites: SOX17 binding residues. C Dual luciferase promoter reporter assay was performed to examine the effects of SOX17 wild type (SOX17-WT) or HMG box deletion (SOX17-ΔHMG) overexpression on promoter activity of NFE2L2 in ESCC cells. D Promoter map for NFE2L2 gene. Regions examined with ChIP assay are marked by red circle-backslash symbol. E ChIP-qPCR assay was performed to measure SOX17 binding ability to the promoter region of NFE2L2 in ESCC cells. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Article Snippet: Japanese ESCC cell line KYSE510 was purchased from the DSMZ-German Collection of Microorganisms and Cell Cultures (Braunschweig, Germany).

Techniques: Plasmid Preparation, Construct, Luciferase, Reporter Assay, Binding Assay, Clone Assay, Over Expression, Activity Assay, ChIP-qPCR

Fig. 3 SOX17 overexpression downregulated NRF2 protein expression and the mRNA level of NRF2-targeted genes. A, B Western blot showed a decreased expression level of NRF2 protein after SOX17-WT overexpression, while no change in NRF2 protein expression after SOX17-ΔHMG overexpression in KYSE510 pair cells (A) and in CE48T pair cells (B). GAPDH was used as an internal control. C and D, The mRNA expressions of NFE2L2 and NRF2-regulated genes GPX2, AKR1C1, AKR1C2, AKR1C3, NQO1, and G6PD were determined by RT-qPCR analysis after SOX17 overexpression for 72 h in KYSE510 pair cells (C) and in CE48T pair cells (D). β-actin was used as an internal control. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Journal: Journal of biomedical science

Article Title: Dysregulation of SOX17/NRF2 axis confers chemoradiotherapy resistance and emerges as a novel therapeutic target in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-022-00873-4

Figure Lengend Snippet: Fig. 3 SOX17 overexpression downregulated NRF2 protein expression and the mRNA level of NRF2-targeted genes. A, B Western blot showed a decreased expression level of NRF2 protein after SOX17-WT overexpression, while no change in NRF2 protein expression after SOX17-ΔHMG overexpression in KYSE510 pair cells (A) and in CE48T pair cells (B). GAPDH was used as an internal control. C and D, The mRNA expressions of NFE2L2 and NRF2-regulated genes GPX2, AKR1C1, AKR1C2, AKR1C3, NQO1, and G6PD were determined by RT-qPCR analysis after SOX17 overexpression for 72 h in KYSE510 pair cells (C) and in CE48T pair cells (D). β-actin was used as an internal control. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Article Snippet: Japanese ESCC cell line KYSE510 was purchased from the DSMZ-German Collection of Microorganisms and Cell Cultures (Braunschweig, Germany).

Techniques: Over Expression, Expressing, Western Blot, Control, Quantitative RT-PCR

Fig. 4 The effects of SOX17 and/or NRF2 overexpression on cell behaviors and tumor growth. A, B Colony formation assay of KYSE510 pair cells manipulated with SOX17 and/or NRF2 expression. The colonies were stained on day 8 after seeding (A), and the colony formation ability was quantified (B). C, D Wound healing assay of KYSE510 pair cells manipulated with SOX17 and/or NRF2 expression. Cells were monitored for their ability to migrate into the wound gap. The wound gap was photographed (C) and quantified (D) at 10 h. E, F Transwell invasion assay of KYSE510 pair cells manipulated with SOX17 and/or NRF2 expression. The invaded cells were photographed (E) and quantified (F) at 20 h. G KYSE510-R cells transfected with SOX17 and/or NRF2 were subcutaneously injected into BALB/c nude mice and observed for tumor growth. H, I Tumor size (H) and tumor weight (I) were measured at the end of the experiment. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Journal: Journal of biomedical science

Article Title: Dysregulation of SOX17/NRF2 axis confers chemoradiotherapy resistance and emerges as a novel therapeutic target in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-022-00873-4

Figure Lengend Snippet: Fig. 4 The effects of SOX17 and/or NRF2 overexpression on cell behaviors and tumor growth. A, B Colony formation assay of KYSE510 pair cells manipulated with SOX17 and/or NRF2 expression. The colonies were stained on day 8 after seeding (A), and the colony formation ability was quantified (B). C, D Wound healing assay of KYSE510 pair cells manipulated with SOX17 and/or NRF2 expression. Cells were monitored for their ability to migrate into the wound gap. The wound gap was photographed (C) and quantified (D) at 10 h. E, F Transwell invasion assay of KYSE510 pair cells manipulated with SOX17 and/or NRF2 expression. The invaded cells were photographed (E) and quantified (F) at 20 h. G KYSE510-R cells transfected with SOX17 and/or NRF2 were subcutaneously injected into BALB/c nude mice and observed for tumor growth. H, I Tumor size (H) and tumor weight (I) were measured at the end of the experiment. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Article Snippet: Japanese ESCC cell line KYSE510 was purchased from the DSMZ-German Collection of Microorganisms and Cell Cultures (Braunschweig, Germany).

Techniques: Over Expression, Colony Assay, Expressing, Staining, Wound Healing Assay, Transwell Invasion Assay, Transfection, Injection

Fig. 5 ZVI@CMC nanoparticles elicited DNMT inhibition to restore the expression of SOX17 and NRF2. A, B Colony formation assay of KYSE510 pair cells treated with ZVI@CMC. The colonies were stained on day 12 after seeding (A), and the colony number was quantified (B). C Intracellular ROS level was determined by flow cytometry analysis of DCFDA fluorescence intensity after ZVI@CMC treatment for 24 h. D Immunoblotting of DNMT1, DNMT3B, SOX17, and NRF2 in ESCC cells treated with ZVI@CMC. GAPDH was used as an internal control. E Immunofluorescence staining of β-TrCP, DNMT1, NRF2, and DAPI in KYSE510 pair cells treated with ZVI@CMC. F Methylation-specific PCR (MSP) demonstrated that ZVI@CMC could reduce the methylation of SOX17 promoter. M indicates methylated PCR products, and U indicates unmethylated PCR products. G RT-qPCR analysis showed that the mRNA expressions of NRF2 downstream genes were downregulated by ZVI@CMC treatment. β-actin was used as an internal control. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Journal: Journal of biomedical science

Article Title: Dysregulation of SOX17/NRF2 axis confers chemoradiotherapy resistance and emerges as a novel therapeutic target in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-022-00873-4

Figure Lengend Snippet: Fig. 5 ZVI@CMC nanoparticles elicited DNMT inhibition to restore the expression of SOX17 and NRF2. A, B Colony formation assay of KYSE510 pair cells treated with ZVI@CMC. The colonies were stained on day 12 after seeding (A), and the colony number was quantified (B). C Intracellular ROS level was determined by flow cytometry analysis of DCFDA fluorescence intensity after ZVI@CMC treatment for 24 h. D Immunoblotting of DNMT1, DNMT3B, SOX17, and NRF2 in ESCC cells treated with ZVI@CMC. GAPDH was used as an internal control. E Immunofluorescence staining of β-TrCP, DNMT1, NRF2, and DAPI in KYSE510 pair cells treated with ZVI@CMC. F Methylation-specific PCR (MSP) demonstrated that ZVI@CMC could reduce the methylation of SOX17 promoter. M indicates methylated PCR products, and U indicates unmethylated PCR products. G RT-qPCR analysis showed that the mRNA expressions of NRF2 downstream genes were downregulated by ZVI@CMC treatment. β-actin was used as an internal control. Data represents mean ± s.e.m. ns: non-significant; *p < 0.05; **p < 0.01; ***p < 0.001

Article Snippet: Japanese ESCC cell line KYSE510 was purchased from the DSMZ-German Collection of Microorganisms and Cell Cultures (Braunschweig, Germany).

Techniques: Inhibition, Expressing, Colony Assay, Staining, Flow Cytometry, Fluorescence, Western Blot, Control, Immunofluorescence, Methylation, Quantitative RT-PCR

Fig. 7 The model of SOX17/NRF2 transcription axis and ZVI@CMC treatment in ESCC. In the CCRT resistant cells, the promoter hypermethylation-induced low SOX17 protein expression causes dysregulation of the cytoprotective enzymes controlled by NRF2, and thus resulting in CCRT resistance (left). Interestingly, ZVI@CMC elicits DNMT inhibition to re-express SOX17 and suppress NRF2-mediated cytoprotective programs in ESCC, and thereby sensitizing cancer cells to CCRT treatment (right)

Journal: Journal of biomedical science

Article Title: Dysregulation of SOX17/NRF2 axis confers chemoradiotherapy resistance and emerges as a novel therapeutic target in esophageal squamous cell carcinoma.

doi: 10.1186/s12929-022-00873-4

Figure Lengend Snippet: Fig. 7 The model of SOX17/NRF2 transcription axis and ZVI@CMC treatment in ESCC. In the CCRT resistant cells, the promoter hypermethylation-induced low SOX17 protein expression causes dysregulation of the cytoprotective enzymes controlled by NRF2, and thus resulting in CCRT resistance (left). Interestingly, ZVI@CMC elicits DNMT inhibition to re-express SOX17 and suppress NRF2-mediated cytoprotective programs in ESCC, and thereby sensitizing cancer cells to CCRT treatment (right)

Article Snippet: Japanese ESCC cell line KYSE510 was purchased from the DSMZ-German Collection of Microorganisms and Cell Cultures (Braunschweig, Germany).

Techniques: Expressing, Inhibition

Association of the upregulation of IBSP expression with the clinicopathological characteristics of patients with ESCC ( n = 269).

Journal: Frontiers in Oncology

Article Title: Upregulation of IBSP Expression Predicts Poor Prognosis in Patients With Esophageal Squamous Cell Carcinoma

doi: 10.3389/fonc.2019.01117

Figure Lengend Snippet: Association of the upregulation of IBSP expression with the clinicopathological characteristics of patients with ESCC ( n = 269).

Article Snippet: The Japanese ESCC cell line KYSE30 was obtained from DSMZ (Braunschweig, Germany), the German Resource Center for Biological Material.

Techniques: Expressing, Cell Differentiation

(A) Dot-plot graph of the fold change in IBSP in ESCC tissues and their adjacent non-tumor tissues. Scatter plots of fold change in IBSP detected by qRT-PCR in ESCC tissues. (B) Representative images of IBSP expression in a pair of ESCC (lower panels) and adjacent normal tissues (upper panels) as detected by immunostaining with the anti-IBSP antibody (brown). The final score of ESCC subgroup is 6 points while that of normal subgroup is 1 point. The slides were counterstained with hematoxylin. Original magnification, ×100 (left), ×200 (right). ** P < 0.01.

Journal: Frontiers in Oncology

Article Title: Upregulation of IBSP Expression Predicts Poor Prognosis in Patients With Esophageal Squamous Cell Carcinoma

doi: 10.3389/fonc.2019.01117

Figure Lengend Snippet: (A) Dot-plot graph of the fold change in IBSP in ESCC tissues and their adjacent non-tumor tissues. Scatter plots of fold change in IBSP detected by qRT-PCR in ESCC tissues. (B) Representative images of IBSP expression in a pair of ESCC (lower panels) and adjacent normal tissues (upper panels) as detected by immunostaining with the anti-IBSP antibody (brown). The final score of ESCC subgroup is 6 points while that of normal subgroup is 1 point. The slides were counterstained with hematoxylin. Original magnification, ×100 (left), ×200 (right). ** P < 0.01.

Article Snippet: The Japanese ESCC cell line KYSE30 was obtained from DSMZ (Braunschweig, Germany), the German Resource Center for Biological Material.

Techniques: Quantitative RT-PCR, Expressing, Immunostaining

Univariate Cox regression analysis of factors possibly influencing disease-specific survival in patients with ESCC.

Journal: Frontiers in Oncology

Article Title: Upregulation of IBSP Expression Predicts Poor Prognosis in Patients With Esophageal Squamous Cell Carcinoma

doi: 10.3389/fonc.2019.01117

Figure Lengend Snippet: Univariate Cox regression analysis of factors possibly influencing disease-specific survival in patients with ESCC.

Article Snippet: The Japanese ESCC cell line KYSE30 was obtained from DSMZ (Braunschweig, Germany), the German Resource Center for Biological Material.

Techniques: Expressing, Cell Differentiation

Multivariate Cox regression analysis of factors possibly influencing disease-specific survival in patients with ESCC.

Journal: Frontiers in Oncology

Article Title: Upregulation of IBSP Expression Predicts Poor Prognosis in Patients With Esophageal Squamous Cell Carcinoma

doi: 10.3389/fonc.2019.01117

Figure Lengend Snippet: Multivariate Cox regression analysis of factors possibly influencing disease-specific survival in patients with ESCC.

Article Snippet: The Japanese ESCC cell line KYSE30 was obtained from DSMZ (Braunschweig, Germany), the German Resource Center for Biological Material.

Techniques: Expressing, Cell Differentiation

Kaplan-Meier plots for the disease-specific survival rate of ESCC patients. (A) Kaplan-Meier plots for the disease-specific survival (DSS) rate of ESCC patients with ( n = 108, green line) or without ( n = 161, blue line) IBSP upregulation. Kaplan-Meier plots for the DSS rate in ESCC patients with or without IBSP upregulation subgrouped into pathologic stage I–II (B) and pathologic stage III (C) .

Journal: Frontiers in Oncology

Article Title: Upregulation of IBSP Expression Predicts Poor Prognosis in Patients With Esophageal Squamous Cell Carcinoma

doi: 10.3389/fonc.2019.01117

Figure Lengend Snippet: Kaplan-Meier plots for the disease-specific survival rate of ESCC patients. (A) Kaplan-Meier plots for the disease-specific survival (DSS) rate of ESCC patients with ( n = 108, green line) or without ( n = 161, blue line) IBSP upregulation. Kaplan-Meier plots for the DSS rate in ESCC patients with or without IBSP upregulation subgrouped into pathologic stage I–II (B) and pathologic stage III (C) .

Article Snippet: The Japanese ESCC cell line KYSE30 was obtained from DSMZ (Braunschweig, Germany), the German Resource Center for Biological Material.

Techniques:

Tumor promoter function of IBSP in ESCC cells. (A) Upregulation of IBSP in ESCC. The expression of IBSP in transfected ESCC cells (ibsp-30) was detected by RT-PCR. ** P < 0.01. (B) The growth curve of IBSP-expressing cells was compared with that of Vec-30 cells by MTT assay. Data points indicate the mean of at least three independent experiments; bars, SD; ** P < 0.05. (C) Representative auxo-action of IBSP in the foci formation of the culture monolayer and quantitative analyses of the foci quantity are shown. Columns indicate means of at least three independent experiments; bars, SD. ** P < 0.05 vs. Vec-30 cells using Student's t -test. (D) The IBSP and Vec-30 cells that invaded through the Matrigel are shown in representative images. The number of invaded tumor cells is quantified in the histogram. Columns indicate means of triplicate experiments; * P < 0.05, ** P < 0.01.

Journal: Frontiers in Oncology

Article Title: Upregulation of IBSP Expression Predicts Poor Prognosis in Patients With Esophageal Squamous Cell Carcinoma

doi: 10.3389/fonc.2019.01117

Figure Lengend Snippet: Tumor promoter function of IBSP in ESCC cells. (A) Upregulation of IBSP in ESCC. The expression of IBSP in transfected ESCC cells (ibsp-30) was detected by RT-PCR. ** P < 0.01. (B) The growth curve of IBSP-expressing cells was compared with that of Vec-30 cells by MTT assay. Data points indicate the mean of at least three independent experiments; bars, SD; ** P < 0.05. (C) Representative auxo-action of IBSP in the foci formation of the culture monolayer and quantitative analyses of the foci quantity are shown. Columns indicate means of at least three independent experiments; bars, SD. ** P < 0.05 vs. Vec-30 cells using Student's t -test. (D) The IBSP and Vec-30 cells that invaded through the Matrigel are shown in representative images. The number of invaded tumor cells is quantified in the histogram. Columns indicate means of triplicate experiments; * P < 0.05, ** P < 0.01.

Article Snippet: The Japanese ESCC cell line KYSE30 was obtained from DSMZ (Braunschweig, Germany), the German Resource Center for Biological Material.

Techniques: Expressing, Transfection, Reverse Transcription Polymerase Chain Reaction, MTT Assay

Figure 1. Low protein expression of SOX17 correlates with poor prognosis and inversely correlates with FN1 protein expression in ESCC patients. (a) Representative IHC of SOX17 protein in four ESCC patients. SOX17 nuclear negative immunoreactivity (2) is found in patient 1 and 2, whereas patient 3 and 4 show SOX17 expression (1) in nuclei of tumor tissue. A fourfold enlarged image of tumor area indicated by arrow is shown in lower left inset for each patient (original magniﬁcation: 2003). (b) Kaplan–Meier curves showing ESCC patients with SOX17 protein low expression had signiﬁcantly poorer overall survival than those with normal expression. (c) IHC of SOX17 and FN1 protein expression level in ESCC tumor tissue array. The representative IHC ﬁgures for SOX17 and FN1 protein are shown for 10 ESCC patients. (d) An inverse correlation between SOX17 and FN1 protein expression was found in 48 ESCC patients analyzed. y axis, percent of cases; x axis, type of comparison. Positive (1) and negative (2) expression status of protein are noted. The percentage in the inverse correlation group (gray columns) and noninverse correlation group (white columns) is indicated above. p values are shown as indicated.

Journal: International journal of cancer

Article Title: Low SOX17 expression is a prognostic factor and drives transcriptional dysregulation and esophageal cancer progression.

doi: 10.1002/ijc.28695

Figure Lengend Snippet: Figure 1. Low protein expression of SOX17 correlates with poor prognosis and inversely correlates with FN1 protein expression in ESCC patients. (a) Representative IHC of SOX17 protein in four ESCC patients. SOX17 nuclear negative immunoreactivity (2) is found in patient 1 and 2, whereas patient 3 and 4 show SOX17 expression (1) in nuclei of tumor tissue. A fourfold enlarged image of tumor area indicated by arrow is shown in lower left inset for each patient (original magniﬁcation: 2003). (b) Kaplan–Meier curves showing ESCC patients with SOX17 protein low expression had signiﬁcantly poorer overall survival than those with normal expression. (c) IHC of SOX17 and FN1 protein expression level in ESCC tumor tissue array. The representative IHC ﬁgures for SOX17 and FN1 protein are shown for 10 ESCC patients. (d) An inverse correlation between SOX17 and FN1 protein expression was found in 48 ESCC patients analyzed. y axis, percent of cases; x axis, type of comparison. Positive (1) and negative (2) expression status of protein are noted. The percentage in the inverse correlation group (gray columns) and noninverse correlation group (white columns) is indicated above. p values are shown as indicated.

Article Snippet: Japanese ESCC cell lines KYSE70, KYSE150 and KYSE510 were purchased from the DSMZ-German Collection of Microorganisms and Cell Cultures (Braunschweig, Germany), where they were characterized by DNA-fingerprinting and isozyme detection.

Techniques: Expressing, Comparison

Figure 2. Overexpression of SOX17 attenuates ESCC cell growth and metastasis in vitro and in vivo. (a) Overexpression of SOX17 attenuates foci formation ability, whereas (b) knockdown of SOX17 promotes foci formation ability in the KYSE510 cells. Western blots showing SOX17 overexpression and si-knockdown in KYSE510 cell. b-actin was used as an internal control. The relative foci formation ability was normal- ized to EV or si-control group. Data represent mean 6 SD from three independent experiments. (c) SOX17 overexpression decreases tumor growth in vivo in ESCC xenograft model. KYSE170-luc cells transfected with EV or SOX17 expression vector were subcutaneously injected into SCID mice and observed for tumor growth. Xenograft images of tumor are shown (n 5 4 mice per group). (d) SOX17 effectively sup- pressed tumor weight compared with EV in SCID mice. (e, f) Transwell migration and invasion assays in two ESCC cells transfected with SOX17 or EV control. The quantitative results showed that SOX17 overexpressing cells migrated or invaded less than vector control cells. Data represent mean 6 SD from three independent experiments. (g) SOX17 overexpression decreases in vivo extravasation and coloniza- tion in ESCC xenograft animal model. The representative lung tissue images of SCID mice intravenously injected with EV and SOX17 expres- sion CE81T cells via tail vein are shown. The red arrows indicate the sites of tumor nodules in the lung tissues (403). Tumor boundaries (red lines) of selected areas are shown (1003). (h) Quantiﬁcation of lung metastatic nodules in EV and SOX17 overexpression groups (n 5 5 mice per group). p values were calculated by two-tailed t test.

Journal: International journal of cancer

Article Title: Low SOX17 expression is a prognostic factor and drives transcriptional dysregulation and esophageal cancer progression.

doi: 10.1002/ijc.28695

Figure Lengend Snippet: Figure 2. Overexpression of SOX17 attenuates ESCC cell growth and metastasis in vitro and in vivo. (a) Overexpression of SOX17 attenuates foci formation ability, whereas (b) knockdown of SOX17 promotes foci formation ability in the KYSE510 cells. Western blots showing SOX17 overexpression and si-knockdown in KYSE510 cell. b-actin was used as an internal control. The relative foci formation ability was normal- ized to EV or si-control group. Data represent mean 6 SD from three independent experiments. (c) SOX17 overexpression decreases tumor growth in vivo in ESCC xenograft model. KYSE170-luc cells transfected with EV or SOX17 expression vector were subcutaneously injected into SCID mice and observed for tumor growth. Xenograft images of tumor are shown (n 5 4 mice per group). (d) SOX17 effectively sup- pressed tumor weight compared with EV in SCID mice. (e, f) Transwell migration and invasion assays in two ESCC cells transfected with SOX17 or EV control. The quantitative results showed that SOX17 overexpressing cells migrated or invaded less than vector control cells. Data represent mean 6 SD from three independent experiments. (g) SOX17 overexpression decreases in vivo extravasation and coloniza- tion in ESCC xenograft animal model. The representative lung tissue images of SCID mice intravenously injected with EV and SOX17 expres- sion CE81T cells via tail vein are shown. The red arrows indicate the sites of tumor nodules in the lung tissues (403). Tumor boundaries (red lines) of selected areas are shown (1003). (h) Quantiﬁcation of lung metastatic nodules in EV and SOX17 overexpression groups (n 5 5 mice per group). p values were calculated by two-tailed t test.

Techniques: Over Expression, In Vitro, In Vivo, Knockdown, Western Blot, Control, Transfection, Expressing, Plasmid Preparation, Injection, Migration, Animal Model, Two Tailed Test

Figure 3. Transcription network and validation of SOX17 transcriptionally regulated genes in ESCC. (a) Interaction network analysis of pro- teins encoded by 489 differentially expressed genes upon SOX17 manipulation. Protein interaction network was generated with STRING 9.05 and visualized with Cytoscape software consisting of 240 proteins connected by 772 protein-protein interactions. GO terms of similar functions are placed into one cluster, which was marked with circles and labels manually. The seven genes for further validation were high- lighted. (b,c) mRNA expression validation of SOX17 transcriptionally regulated genes in KYSE170-luc cell and KYSE510 cell. SOX17 protein expression was examined by Western blot (left). The qRT-PCR results showing the mRNA expression level of seven SOX17 transcriptionally regulated candidate genes (MACC1, MALAT1, NBN, NFAT5, CSNK1A1, FN1 and SERBP1) was decreased in cells overexpressing wild-type SOX17 (SOX17-WT, black bars), whereas the transcriptional suppression was attenuated in the HMG box-deleted SOX17 cells (SOX17- DHMG, gray bars). Relative mRNA expression fold change is indicated on the y-axis, and the type of comparison is plotted on the x-axis. p values were calculated by two-tailed t test for three independent experiments as indicated. [Color ﬁgure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

Journal: International journal of cancer

Article Title: Low SOX17 expression is a prognostic factor and drives transcriptional dysregulation and esophageal cancer progression.

doi: 10.1002/ijc.28695

Figure Lengend Snippet: Figure 3. Transcription network and validation of SOX17 transcriptionally regulated genes in ESCC. (a) Interaction network analysis of pro- teins encoded by 489 differentially expressed genes upon SOX17 manipulation. Protein interaction network was generated with STRING 9.05 and visualized with Cytoscape software consisting of 240 proteins connected by 772 protein-protein interactions. GO terms of similar functions are placed into one cluster, which was marked with circles and labels manually. The seven genes for further validation were high- lighted. (b,c) mRNA expression validation of SOX17 transcriptionally regulated genes in KYSE170-luc cell and KYSE510 cell. SOX17 protein expression was examined by Western blot (left). The qRT-PCR results showing the mRNA expression level of seven SOX17 transcriptionally regulated candidate genes (MACC1, MALAT1, NBN, NFAT5, CSNK1A1, FN1 and SERBP1) was decreased in cells overexpressing wild-type SOX17 (SOX17-WT, black bars), whereas the transcriptional suppression was attenuated in the HMG box-deleted SOX17 cells (SOX17- DHMG, gray bars). Relative mRNA expression fold change is indicated on the y-axis, and the type of comparison is plotted on the x-axis. p values were calculated by two-tailed t test for three independent experiments as indicated. [Color ﬁgure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

Techniques: Biomarker Discovery, Generated, Software, Protein-Protein interactions, Expressing, Western Blot, Quantitative RT-PCR, Comparison, Two Tailed Test

Figure 5. Re-expression of FN1 (a, b) or MACC1 (c, d) restores cell migration and invasion ability in ESCC cells overexpressing wild-type SOX17. Left: Transwell-invasion (2003 magniﬁcation) and transwell-migration (403 magniﬁcation) assays of KYSE170-luc and KYSE510 cells transfected with EV control, SOX17-WT, SOX17-DHMG or both SOX17-WT and the target gene indicated; Right: The quantitative results showed that low cell motility in SOX17-WT cells (black bar) can be reversed by cotransfection with FN1 or MACC1 (dark gray bar). p values were calculated by two-tailed t test. Data represent mean 6 SD from three independent experiments. [Color ﬁgure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

Journal: International journal of cancer

Article Title: Low SOX17 expression is a prognostic factor and drives transcriptional dysregulation and esophageal cancer progression.

doi: 10.1002/ijc.28695

Figure Lengend Snippet: Figure 5. Re-expression of FN1 (a, b) or MACC1 (c, d) restores cell migration and invasion ability in ESCC cells overexpressing wild-type SOX17. Left: Transwell-invasion (2003 magniﬁcation) and transwell-migration (403 magniﬁcation) assays of KYSE170-luc and KYSE510 cells transfected with EV control, SOX17-WT, SOX17-DHMG or both SOX17-WT and the target gene indicated; Right: The quantitative results showed that low cell motility in SOX17-WT cells (black bar) can be reversed by cotransfection with FN1 or MACC1 (dark gray bar). p values were calculated by two-tailed t test. Data represent mean 6 SD from three independent experiments. [Color ﬁgure can be viewed in the online issue, which is available at wileyonlinelibrary.com.]

Techniques: Expressing, Migration, Transfection, Control, Cotransfection, Two Tailed Test

Figure 1. ADAR1 is signiﬁcantly overexpressed in primary ESCC samples and its clinical implication. A, box plots represent the relative ADAR1 (left) and ADAR2 (right) expression levels in 69 matched pairs of ESCC and nontumor specimens in cohort 1. The data are presented as box plots with the median (horizontal line), 25% to 75% (box), and 5% to 95% (error bar) percentiles for each group. B, Western blot analyses of ADAR1 and ADAR2 expression levels in six paired ESCC and nontumor specimens in cohort 1. GAPDH was used as a loading control. C, example of the ADAR1 expression level detected in a matched pair of primary ESCC and nontumor tissue in cohort 2. The boxed regions are magniﬁed and displayed in the bottom panels. Scale bar, 200 mm. D, Kaplan–Meier plots for the overall survival rate of patients with (n ¼ 90, red line) or without (n ¼ 46, blue line) the tumoral overexpression of ADAR1. E, FISH analysis of the ADAR1 gene (red signal) and the control chromosome 1 centromere probe (green signal) speciﬁcally hybridized to the chromosome 1 (indicated by white arrow) of normal human karyotype (left). A representative example of ADAR1 gene ampliﬁcation (red signals) in a matched pair of primary ESCC and nontumor tissue (middle and right panels). Scale bar, 500 mm.

Journal: Cancer Research

Article Title: Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma

doi: 10.1158/0008-5472.can-13-2545

Figure Lengend Snippet: Figure 1. ADAR1 is signiﬁcantly overexpressed in primary ESCC samples and its clinical implication. A, box plots represent the relative ADAR1 (left) and ADAR2 (right) expression levels in 69 matched pairs of ESCC and nontumor specimens in cohort 1. The data are presented as box plots with the median (horizontal line), 25% to 75% (box), and 5% to 95% (error bar) percentiles for each group. B, Western blot analyses of ADAR1 and ADAR2 expression levels in six paired ESCC and nontumor specimens in cohort 1. GAPDH was used as a loading control. C, example of the ADAR1 expression level detected in a matched pair of primary ESCC and nontumor tissue in cohort 2. The boxed regions are magniﬁed and displayed in the bottom panels. Scale bar, 200 mm. D, Kaplan–Meier plots for the overall survival rate of patients with (n ¼ 90, red line) or without (n ¼ 46, blue line) the tumoral overexpression of ADAR1. E, FISH analysis of the ADAR1 gene (red signal) and the control chromosome 1 centromere probe (green signal) speciﬁcally hybridized to the chromosome 1 (indicated by white arrow) of normal human karyotype (left). A representative example of ADAR1 gene ampliﬁcation (red signals) in a matched pair of primary ESCC and nontumor tissue (middle and right panels). Scale bar, 500 mm.

Article Snippet: Six Japanese ESCC cell lines (KYSE140, KYSE410, KYSE180, KYSE30, KYSE510, and KYSE520) were obtained from DSMZ, the German Resource Centre for Biological Material (11).

Techniques: Expressing, Western Blot, Control, Over Expression

Figure 2. ADAR1 functions as an oncogene during ESCC progression. A, Western blot analyses showing expression of ADAR1 and ADAR2 proteins in the indicated cell lines. b-actin was the loading control. B, cell growth rates of the indicated cell lines were compared by XTT assays. The results are expressed as the mean SD of triplicate wells within the same experiment (, P < 0.05; , P < 0.01; , P < 0.001, unpaired, two-tailed Student t test). C, quantiﬁcation of foci formation induced by the indicated stable cell lines. Triplicate independent experiments were performed and the data were expressed as the mean SD of triplicate wells within the same experiment (, P < 0.05; , P < 0.001, unpaired, two-tailed Student t test). Scale bar, 0.5 cm. D, quantiﬁcation of colonies (formed in soft agar) that were induced by the indicated cell lines. (Continued on the following page.)

Journal: Cancer Research

Article Title: Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma

doi: 10.1158/0008-5472.can-13-2545

Figure Lengend Snippet: Figure 2. ADAR1 functions as an oncogene during ESCC progression. A, Western blot analyses showing expression of ADAR1 and ADAR2 proteins in the indicated cell lines. b-actin was the loading control. B, cell growth rates of the indicated cell lines were compared by XTT assays. The results are expressed as the mean SD of triplicate wells within the same experiment (, P < 0.05; , P < 0.01; , P < 0.001, unpaired, two-tailed Student t test). C, quantiﬁcation of foci formation induced by the indicated stable cell lines. Triplicate independent experiments were performed and the data were expressed as the mean SD of triplicate wells within the same experiment (, P < 0.05; , P < 0.001, unpaired, two-tailed Student t test). Scale bar, 0.5 cm. D, quantiﬁcation of colonies (formed in soft agar) that were induced by the indicated cell lines. (Continued on the following page.)

Article Snippet: Six Japanese ESCC cell lines (KYSE140, KYSE410, KYSE180, KYSE30, KYSE510, and KYSE520) were obtained from DSMZ, the German Resource Centre for Biological Material (11).

Techniques: Western Blot, Expressing, Control, Two Tailed Test, Stable Transfection

Figure 4. The hyperediting patterns of AZIN1 and FLNB transcripts induced by the upregulation of ADAR1 in ESCC tumors. A, line-bar chart showing the editing levels of AZIN1 and FLNB as well as the expression level of ADAR1 in nine ESCC cell lines. B, the AZIN1 (left) and FLNB (right) editing levels in 69 paired ESCC and matched nontumor specimens in cohort 1 (paired Student t test). C, correlation between the expression level of ADAR1 and the editing level of AZIN1 (left) or FLNB (right) in 69 paired ESCC and matched nontumor specimens in cohort 1. D and E, sequence chromatograms of the AZIN1 and FLNB transcripts in EC109 (D) or KYSE180 (E) cells that transiently transduced with an ADAR1 p110 lentivirus (þADAR1 p110) or LacZ control lentivirus (þcontrol). The percentages of edited AZIN1 and FLNB transcripts were detected as described in Materials and Methods. Arrow, the editing position. F, sequence chromatograms of theAZIN1 andFLNB transcripts inKYSE510 cells (E) that were transiently transfected with two shRNAs against ADAR1 gene (shAR1#5 and shAR1 #7) or the control shRNA (control). Arrow, the editing position.

Journal: Cancer Research

Article Title: Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma

doi: 10.1158/0008-5472.can-13-2545

Figure Lengend Snippet: Figure 4. The hyperediting patterns of AZIN1 and FLNB transcripts induced by the upregulation of ADAR1 in ESCC tumors. A, line-bar chart showing the editing levels of AZIN1 and FLNB as well as the expression level of ADAR1 in nine ESCC cell lines. B, the AZIN1 (left) and FLNB (right) editing levels in 69 paired ESCC and matched nontumor specimens in cohort 1 (paired Student t test). C, correlation between the expression level of ADAR1 and the editing level of AZIN1 (left) or FLNB (right) in 69 paired ESCC and matched nontumor specimens in cohort 1. D and E, sequence chromatograms of the AZIN1 and FLNB transcripts in EC109 (D) or KYSE180 (E) cells that transiently transduced with an ADAR1 p110 lentivirus (þADAR1 p110) or LacZ control lentivirus (þcontrol). The percentages of edited AZIN1 and FLNB transcripts were detected as described in Materials and Methods. Arrow, the editing position. F, sequence chromatograms of theAZIN1 andFLNB transcripts inKYSE510 cells (E) that were transiently transfected with two shRNAs against ADAR1 gene (shAR1#5 and shAR1 #7) or the control shRNA (control). Arrow, the editing position.

Article Snippet: Six Japanese ESCC cell lines (KYSE140, KYSE410, KYSE180, KYSE30, KYSE510, and KYSE520) were obtained from DSMZ, the German Resource Centre for Biological Material (11).

Techniques: Expressing, Sequencing, Transduction, Control, Transfection, shRNA

Figure 5. The edited AZIN1 confers more aggressive tumorigenic phenotypes during ESCC progression. A, sequence chromatograms of the AZIN1 transcript in the indicated cell lines. Arrow, the editing position. B, cell growth rates of the indicated cell lines were compared by XTT assays. The results are expressed as described above (, P < 0.05; , P < 0.001). C, quantiﬁcation of foci formation induced by the indicated stable cell lines. Triplicate independent experiments were performed and the data were expressed as described above (, P < 0.01; , P < 0.001). Scale bar, 0.5 cm. D, quantiﬁcation of colonies (formed in soft agar) that were induced by the indicated cell lines. Triplicate independent experiments were performed and the data were expressed as described above (, P < 0.05; , P < 0.01). Scale bar, 200 mm. E, quantiﬁcation of cells from the indicated cells that migrated through the PET-membrane or invaded through the Matrigel-coated membrane. (, P < 0.05; , P < 0.01; , P < 0.001, unpaired, two-tailed Student t test). Scale bar, 200 mm. F, growth curves of tumors derived from the indicated cell lines over a period of 4 weeks. Data are presented as the mean SD (n ¼ 6, , P < 0.05; , P < 0.001; unpaired, two-tailed Student t test).

Journal: Cancer Research

Article Title: Adenosine-to-Inosine RNA Editing Mediated by ADARs in Esophageal Squamous Cell Carcinoma

doi: 10.1158/0008-5472.can-13-2545

Figure Lengend Snippet: Figure 5. The edited AZIN1 confers more aggressive tumorigenic phenotypes during ESCC progression. A, sequence chromatograms of the AZIN1 transcript in the indicated cell lines. Arrow, the editing position. B, cell growth rates of the indicated cell lines were compared by XTT assays. The results are expressed as described above (, P < 0.05; , P < 0.001). C, quantiﬁcation of foci formation induced by the indicated stable cell lines. Triplicate independent experiments were performed and the data were expressed as described above (, P < 0.01; , P < 0.001). Scale bar, 0.5 cm. D, quantiﬁcation of colonies (formed in soft agar) that were induced by the indicated cell lines. Triplicate independent experiments were performed and the data were expressed as described above (, P < 0.05; , P < 0.01). Scale bar, 200 mm. E, quantiﬁcation of cells from the indicated cells that migrated through the PET-membrane or invaded through the Matrigel-coated membrane. (, P < 0.05; , P < 0.01; , P < 0.001, unpaired, two-tailed Student t test). Scale bar, 200 mm. F, growth curves of tumors derived from the indicated cell lines over a period of 4 weeks. Data are presented as the mean SD (n ¼ 6, , P < 0.05; , P < 0.001; unpaired, two-tailed Student t test).

Article Snippet: Six Japanese ESCC cell lines (KYSE140, KYSE410, KYSE180, KYSE30, KYSE510, and KYSE520) were obtained from DSMZ, the German Resource Centre for Biological Material (11).

Techniques: Sequencing, Stable Transfection, Membrane, Two Tailed Test, Derivative Assay

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