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786o cells (ATCC)

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ATCC 786o cells

PDLIM1 knockdown reduces proliferation, clonogenicity, and migration in renal cancer cells in vitro. (A) qPCR validation of siRNA/shRNA‑mediated PDLIM1 knockdown in renal cancer cell lines (786‑O and OSRC-2). (B) CCK‑8 proliferation/viability curves comparing control and PDLIM1‑depleted cells over time. (C-D) Representative images (C) and quantification (D) of wound‑healing assays. (E) Transwell migration assays showing decreased motility/invasiveness after PDLIM1 depletion. (F) Quantification of transwell migration assays. Data are presented as mean ± SEM; statistical significance was determined by two‑sided Student’s t‑test (two groups) or one‑way ANOVA with Tukey’s post hoc test (multiple groups), unless otherwise specified. ns, not significant; * FDR < 0.05; ** FDR < 0.01; *** FDR < 0.001.

786o Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 2188 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/786o cells/product/ATCC
Average 98 stars, based on 2188 article reviews

786o cells - by Bioz Stars, 2026-05

98/100 stars

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1) Product Images from "Integrated spatial and single‑cell transcriptomics maps disulfidptosis in renal cell carcinoma and reveals PDLIM1 as a prognostic biomarker and potential therapeutic target"

Article Title: Integrated spatial and single‑cell transcriptomics maps disulfidptosis in renal cell carcinoma and reveals PDLIM1 as a prognostic biomarker and potential therapeutic target

Journal: Translational Oncology

doi: 10.1016/j.tranon.2026.102765

Figure Legend Snippet: PDLIM1 knockdown reduces proliferation, clonogenicity, and migration in renal cancer cells in vitro. (A) qPCR validation of siRNA/shRNA‑mediated PDLIM1 knockdown in renal cancer cell lines (786‑O and OSRC-2). (B) CCK‑8 proliferation/viability curves comparing control and PDLIM1‑depleted cells over time. (C-D) Representative images (C) and quantification (D) of wound‑healing assays. (E) Transwell migration assays showing decreased motility/invasiveness after PDLIM1 depletion. (F) Quantification of transwell migration assays. Data are presented as mean ± SEM; statistical significance was determined by two‑sided Student’s t‑test (two groups) or one‑way ANOVA with Tukey’s post hoc test (multiple groups), unless otherwise specified. ns, not significant; * FDR < 0.05; ** FDR < 0.01; *** FDR < 0.001.

Techniques Used: Knockdown, Migration, In Vitro, Biomarker Discovery, Control

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Journal: Translational Oncology

Article Title: Integrated spatial and single‑cell transcriptomics maps disulfidptosis in renal cell carcinoma and reveals PDLIM1 as a prognostic biomarker and potential therapeutic target

doi: 10.1016/j.tranon.2026.102765

Figure Lengend Snippet: PDLIM1 knockdown reduces proliferation, clonogenicity, and migration in renal cancer cells in vitro. (A) qPCR validation of siRNA/shRNA‑mediated PDLIM1 knockdown in renal cancer cell lines (786‑O and OSRC-2). (B) CCK‑8 proliferation/viability curves comparing control and PDLIM1‑depleted cells over time. (C-D) Representative images (C) and quantification (D) of wound‑healing assays. (E) Transwell migration assays showing decreased motility/invasiveness after PDLIM1 depletion. (F) Quantification of transwell migration assays. Data are presented as mean ± SEM; statistical significance was determined by two‑sided Student’s t‑test (two groups) or one‑way ANOVA with Tukey’s post hoc test (multiple groups), unless otherwise specified. ns, not significant; * FDR < 0.05; ** FDR < 0.01; *** FDR < 0.001.

Article Snippet: 786O cells and OSRC2 cells were provided by ATCC.

Techniques: Knockdown, Migration, In Vitro, Biomarker Discovery, Control

NRP2 promotes resistance to sorafenib in ccRCC. (A) Venn analysis was performed for genes highly expressed in sorafenib resistance groups of GSE64052 , GSE225537 , GSE242333 and GSE213615 . (B) Determination of sorafenib IC50 in 786O and Caki-1 cells. (C) NRP2 mRNA expression was identified in the control group and in sorafenib resistant 768O and AKI-1 cells. (D) NRP2 protein expression was identified in the control group and in sorafenib resistant 768O and AKI-1 cells. (E) Determination of sorafenib IC50 in 786O and Caki-1 cells with NRP2 overexpression. (F) Determination of sorafenib IC50 in 786O and Caki-1 cells with NRP2 knockout. (G) The expression of NRP2 mRNA in the 786O and Caki-1 treated as shown was detected by qRT-PCR. (H) The expression of NRP2 protein in the 786O and Caki-1 treated as shown was detected by WB. (I) CCK8 cell proliferation assay was used to detect differences about proliferation of the cells treated as shown. (J) Colony formation assay was used to detect differences about proliferation of the cells treated as shown. (K) Transwell assay was used to detect differences about metastasis of the cells treated as shown. Scale bar, 400 μm. (L) Transwell assay was used to detect differences about invasion of the cells treated as shown. Scale bar, 400 μm. (M) Representative photographs of xenograft tumors of shNRP2+Sor and shNRP2+DMSO. (N) The weight of xenograft tumors of shNRP2+Sor and shNRP2+DMSO. (O) The growth volume of xenograft tumors of shNRP2+Sor and shNRP2+DMSO. Statistics (B, E, F): Dose-response curves were fit with a four-parameter logistic model; IC 50 compared by extra sum-of-squares F tests on log(IC 50 ); two-sided. Statistics (I-L): One-way ANOVA with Dunnett (vs control) or Tukey (all pairwise); for matched designs, repeated-measures ANOVA/mixed-effects (REML); Holm-Sidak correction.

Journal: American Journal of Cancer Research

Article Title: Neuropilin-2 (NRP2) mediates sorafenib resistance in clear cell renal cell carcinoma via the NRP2/NF-κB/TNFα axis

doi: 10.62347/GNKC8489

Figure Lengend Snippet: NRP2 promotes resistance to sorafenib in ccRCC. (A) Venn analysis was performed for genes highly expressed in sorafenib resistance groups of GSE64052 , GSE225537 , GSE242333 and GSE213615 . (B) Determination of sorafenib IC50 in 786O and Caki-1 cells. (C) NRP2 mRNA expression was identified in the control group and in sorafenib resistant 768O and AKI-1 cells. (D) NRP2 protein expression was identified in the control group and in sorafenib resistant 768O and AKI-1 cells. (E) Determination of sorafenib IC50 in 786O and Caki-1 cells with NRP2 overexpression. (F) Determination of sorafenib IC50 in 786O and Caki-1 cells with NRP2 knockout. (G) The expression of NRP2 mRNA in the 786O and Caki-1 treated as shown was detected by qRT-PCR. (H) The expression of NRP2 protein in the 786O and Caki-1 treated as shown was detected by WB. (I) CCK8 cell proliferation assay was used to detect differences about proliferation of the cells treated as shown. (J) Colony formation assay was used to detect differences about proliferation of the cells treated as shown. (K) Transwell assay was used to detect differences about metastasis of the cells treated as shown. Scale bar, 400 μm. (L) Transwell assay was used to detect differences about invasion of the cells treated as shown. Scale bar, 400 μm. (M) Representative photographs of xenograft tumors of shNRP2+Sor and shNRP2+DMSO. (N) The weight of xenograft tumors of shNRP2+Sor and shNRP2+DMSO. (O) The growth volume of xenograft tumors of shNRP2+Sor and shNRP2+DMSO. Statistics (B, E, F): Dose-response curves were fit with a four-parameter logistic model; IC 50 compared by extra sum-of-squares F tests on log(IC 50 ); two-sided. Statistics (I-L): One-way ANOVA with Dunnett (vs control) or Tukey (all pairwise); for matched designs, repeated-measures ANOVA/mixed-effects (REML); Holm-Sidak correction.

Article Snippet: Renal clear cell cancer cell lines 786O and AKI-1 were both derived from the American Type Culture Collection (ATCC) and cultured at 37°C and 5% CO 2 .

Techniques: Expressing, Control, Over Expression, Knock-Out, Quantitative RT-PCR, Proliferation Assay, Colony Assay, Transwell Assay

NRP2 promotes proliferation, metastasis and invasion of 786O and Caki-1. (A) The expression of NRP2 mRNA in the 786O and Caki-1 treated as shown was detected by qRT-PCR. (B) The expression of NRP2 protein in the 786O and Caki-1 treated as shown was detected by WB. (C) CCK8 cell proliferation assay was used to detect differences about proliferation of the cells treated as shown. (D) Colony formation assay was used to detect differences about proliferation of the cells treated as shown. (E) Transwell assay was used to detect differences about metastasis of the cells treated as shown. Scale bar, 400 μm. (F) Transwell assay was used to detect differences about invasion of the cells treated as shown. Scale bar, 400 μm. Statistics (C-F): Within a single cell line: one-way ANOVA + Dunnett/Tukey. For cell line × treatment designs: two-way ANOVA with interaction + Sidak/Tukey; repeated-measures ANOVA/REML when matched; Holm-Sidak correction.

Journal: American Journal of Cancer Research

Article Title: Neuropilin-2 (NRP2) mediates sorafenib resistance in clear cell renal cell carcinoma via the NRP2/NF-κB/TNFα axis

doi: 10.62347/GNKC8489

Figure Lengend Snippet: NRP2 promotes proliferation, metastasis and invasion of 786O and Caki-1. (A) The expression of NRP2 mRNA in the 786O and Caki-1 treated as shown was detected by qRT-PCR. (B) The expression of NRP2 protein in the 786O and Caki-1 treated as shown was detected by WB. (C) CCK8 cell proliferation assay was used to detect differences about proliferation of the cells treated as shown. (D) Colony formation assay was used to detect differences about proliferation of the cells treated as shown. (E) Transwell assay was used to detect differences about metastasis of the cells treated as shown. Scale bar, 400 μm. (F) Transwell assay was used to detect differences about invasion of the cells treated as shown. Scale bar, 400 μm. Statistics (C-F): Within a single cell line: one-way ANOVA + Dunnett/Tukey. For cell line × treatment designs: two-way ANOVA with interaction + Sidak/Tukey; repeated-measures ANOVA/REML when matched; Holm-Sidak correction.

Article Snippet: Renal clear cell cancer cell lines 786O and AKI-1 were both derived from the American Type Culture Collection (ATCC) and cultured at 37°C and 5% CO 2 .

Techniques: Expressing, Quantitative RT-PCR, Proliferation Assay, Colony Assay, Transwell Assay

NRP2 promotes TNF-α signaling via NF-κB. (A) Venn analysis was performed for signaling enhanced in NRP2 overexpression or sorafenib resistance groups of KIRC, GSE64052 , GSE225537 and GSE242333 . (B) The variation in enrichmentScore among KIRC, GSE64052 , GSE225537 , and GSE242333 within the TNF-α signaling via NF-κB and IL2 STAT5 signaling pathways. (C) The variation in NSE among KIRC, GSE64052 , GSE225537 , and GSE242333 within the TNF-α signaling via NF-κB and IL2 STAT5 signaling pathways. (D) The expression of p65, p-p65 and TNFα in 786O and Caki-1 cells with NRP2 overexpression was detected by WB. (E) The expression of p65, p-p65 and TNFα in 786O and Caki-1 cells with NRP2 knockout was detected by WB. (F) The expression of p65, p-p65 and TNFα in 786O and Caki-1 cells with sorafenib resistance was detected by WB. Statistics (D-F): Two-way ANOVA (cell line × treatment) with main effects and interaction reported; Sidak post hoc tests; two-sided.

Journal: American Journal of Cancer Research

Article Title: Neuropilin-2 (NRP2) mediates sorafenib resistance in clear cell renal cell carcinoma via the NRP2/NF-κB/TNFα axis

doi: 10.62347/GNKC8489

Figure Lengend Snippet: NRP2 promotes TNF-α signaling via NF-κB. (A) Venn analysis was performed for signaling enhanced in NRP2 overexpression or sorafenib resistance groups of KIRC, GSE64052 , GSE225537 and GSE242333 . (B) The variation in enrichmentScore among KIRC, GSE64052 , GSE225537 , and GSE242333 within the TNF-α signaling via NF-κB and IL2 STAT5 signaling pathways. (C) The variation in NSE among KIRC, GSE64052 , GSE225537 , and GSE242333 within the TNF-α signaling via NF-κB and IL2 STAT5 signaling pathways. (D) The expression of p65, p-p65 and TNFα in 786O and Caki-1 cells with NRP2 overexpression was detected by WB. (E) The expression of p65, p-p65 and TNFα in 786O and Caki-1 cells with NRP2 knockout was detected by WB. (F) The expression of p65, p-p65 and TNFα in 786O and Caki-1 cells with sorafenib resistance was detected by WB. Statistics (D-F): Two-way ANOVA (cell line × treatment) with main effects and interaction reported; Sidak post hoc tests; two-sided.

Article Snippet: Renal clear cell cancer cell lines 786O and AKI-1 were both derived from the American Type Culture Collection (ATCC) and cultured at 37°C and 5% CO 2 .

Techniques: Over Expression, Protein-Protein interactions, Expressing, Knock-Out

NRP2-mediated proliferation, metastasis, and invasion depend in part on TNFα. (A) The expression of NRP2 mRNA in the 786O and Caki-1 treated as shown was detected by qRT-PCR. (B) The expression of NRP2 protein in the 786O and Caki-1 treated as shown was detected by WB. (C) CCK8 cell proliferation assay was used to detect differences about proliferation of the cells treated as shown. (D) Colony formation assay was used to detect differences about proliferation of the cells treated as shown. (E) Transwell assay was used to detect differences about metastasis of the cells treated as shown. Scale bar, 400 μm. (F) Transwell assay was used to detect differences about invasion of the cells treated as shown. Scale bar, 400 μm. Statistics (C-F): Two-way ANOVA with interaction assessed for combination effects; Sidak post hoc tests; two-sided.

Journal: American Journal of Cancer Research

Article Title: Neuropilin-2 (NRP2) mediates sorafenib resistance in clear cell renal cell carcinoma via the NRP2/NF-κB/TNFα axis

doi: 10.62347/GNKC8489

Figure Lengend Snippet: NRP2-mediated proliferation, metastasis, and invasion depend in part on TNFα. (A) The expression of NRP2 mRNA in the 786O and Caki-1 treated as shown was detected by qRT-PCR. (B) The expression of NRP2 protein in the 786O and Caki-1 treated as shown was detected by WB. (C) CCK8 cell proliferation assay was used to detect differences about proliferation of the cells treated as shown. (D) Colony formation assay was used to detect differences about proliferation of the cells treated as shown. (E) Transwell assay was used to detect differences about metastasis of the cells treated as shown. Scale bar, 400 μm. (F) Transwell assay was used to detect differences about invasion of the cells treated as shown. Scale bar, 400 μm. Statistics (C-F): Two-way ANOVA with interaction assessed for combination effects; Sidak post hoc tests; two-sided.

Article Snippet: Renal clear cell cancer cell lines 786O and AKI-1 were both derived from the American Type Culture Collection (ATCC) and cultured at 37°C and 5% CO 2 .

Techniques: Expressing, Quantitative RT-PCR, Proliferation Assay, Colony Assay, Transwell Assay

Adalimumab reverses 786O and Caki-1 cells resistance to sorafenib. (A) CCK8 cell proliferation assay was used to detect differences about proliferation of the cells treated as shown. (B) Colony formation assay was used to detect differences about proliferation of the cells treated as shown. (C) Transwell assay was used to detect differences about metastasis of the cells treated as shown. Scale bar, 400 μm. (D) Transwell assay was used to detect differences about invasion of the cells treated as shown. Scale bar, 400 μm. Statistics (A-D): Two-way ANOVA; for repeated measures, repeated-measures two-way ANOVA or mixed-effects (REML); Sidak/Tukey post hoc tests; two-sided.

Journal: American Journal of Cancer Research

Article Title: Neuropilin-2 (NRP2) mediates sorafenib resistance in clear cell renal cell carcinoma via the NRP2/NF-κB/TNFα axis

doi: 10.62347/GNKC8489

Figure Lengend Snippet: Adalimumab reverses 786O and Caki-1 cells resistance to sorafenib. (A) CCK8 cell proliferation assay was used to detect differences about proliferation of the cells treated as shown. (B) Colony formation assay was used to detect differences about proliferation of the cells treated as shown. (C) Transwell assay was used to detect differences about metastasis of the cells treated as shown. Scale bar, 400 μm. (D) Transwell assay was used to detect differences about invasion of the cells treated as shown. Scale bar, 400 μm. Statistics (A-D): Two-way ANOVA; for repeated measures, repeated-measures two-way ANOVA or mixed-effects (REML); Sidak/Tukey post hoc tests; two-sided.

Article Snippet: Renal clear cell cancer cell lines 786O and AKI-1 were both derived from the American Type Culture Collection (ATCC) and cultured at 37°C and 5% CO 2 .

Techniques: Proliferation Assay, Colony Assay, Transwell Assay

Identification of 11 Important DEGs in ccRCC. (A) Venn diagram of genes in the TCGA and DEPMap datasets. (B) Expression heatmap of the eleven genes in normal versus tumor samples. (C) Differential expression levels of the eleven genes in normal and tumor samples. (D) Locations of the DEGs on chromosomes. (E) Expression correlation analysis of the eleven DEGs. *p < 0.05; **p < 0.01; ***p < 0.001.

Journal: Frontiers in Immunology

Article Title: CRISPR/Cas9-based discovery of ccRCC therapeutic opportunities through molecular mechanism and immune microenvironment analysis

doi: 10.3389/fimmu.2025.1619361

Figure Lengend Snippet: Identification of 11 Important DEGs in ccRCC. (A) Venn diagram of genes in the TCGA and DEPMap datasets. (B) Expression heatmap of the eleven genes in normal versus tumor samples. (C) Differential expression levels of the eleven genes in normal and tumor samples. (D) Locations of the DEGs on chromosomes. (E) Expression correlation analysis of the eleven DEGs. *p < 0.05; **p < 0.01; ***p < 0.001.

Article Snippet: The ccRCC cell lines 786O, 769P, and Caki-1 were obtained from the American Type Culture Collection (ATCC).

Techniques: Expressing, Quantitative Proteomics

Multi method validation of risk score-derived prognostic models. (A) KM survival curves demonstrated markedly shorter overall survival in high-risk ccRCC patients relative to those in the low-risk group. (B) ROC analysis of the DEGs prognostic signature for predicting the 1/3/5-year survival. (C, D) Risk score stratification and survival duration distribution in ccRCC cohort. (E) PCA discriminates high- and low-risk groups using whole transcriptome data. (F) KM survival analysis of ccRCC patients stratified by risk score in the GEO validation cohort ( GSE26909 , n=39).

Journal: Frontiers in Immunology

Article Title: CRISPR/Cas9-based discovery of ccRCC therapeutic opportunities through molecular mechanism and immune microenvironment analysis

doi: 10.3389/fimmu.2025.1619361

Figure Lengend Snippet: Multi method validation of risk score-derived prognostic models. (A) KM survival curves demonstrated markedly shorter overall survival in high-risk ccRCC patients relative to those in the low-risk group. (B) ROC analysis of the DEGs prognostic signature for predicting the 1/3/5-year survival. (C, D) Risk score stratification and survival duration distribution in ccRCC cohort. (E) PCA discriminates high- and low-risk groups using whole transcriptome data. (F) KM survival analysis of ccRCC patients stratified by risk score in the GEO validation cohort ( GSE26909 , n=39).

Article Snippet: The ccRCC cell lines 786O, 769P, and Caki-1 were obtained from the American Type Culture Collection (ATCC).

Techniques: Biomarker Discovery, Derivative Assay

Construction of a nomogram for prediction prognosis. (A) Univariate Cox regression analysis identified grade, stage, T stage, M stage, and risk score as significant prognostic factors. (B) Multivariate Cox regression identifies risk score and age as independent prognostic predictors. (C) Prognostic nomogram incorporating risk score and age for ccRCC survival probability. (D–F) Calibration curves demonstrate the accuracy of 1-year, 3-year, and 5-year overall survival predictions.

Journal: Frontiers in Immunology

Article Title: CRISPR/Cas9-based discovery of ccRCC therapeutic opportunities through molecular mechanism and immune microenvironment analysis

doi: 10.3389/fimmu.2025.1619361

Figure Lengend Snippet: Construction of a nomogram for prediction prognosis. (A) Univariate Cox regression analysis identified grade, stage, T stage, M stage, and risk score as significant prognostic factors. (B) Multivariate Cox regression identifies risk score and age as independent prognostic predictors. (C) Prognostic nomogram incorporating risk score and age for ccRCC survival probability. (D–F) Calibration curves demonstrate the accuracy of 1-year, 3-year, and 5-year overall survival predictions.

Article Snippet: The ccRCC cell lines 786O, 769P, and Caki-1 were obtained from the American Type Culture Collection (ATCC).

Techniques:

Correlation of immune microenvironment with risk score. (A) Immune cell infiltration landscape in ccRCC revealed by CIBERSORT. (B–F) Linear regression models demonstrate risk score-dependent immune cell infiltration patterns. (G) Differential immune cell distribution between risk groups. (H–J) Risk-stratified therapeutic sensitivity to pazopanib, sunitinib, and temsirolimus.

Journal: Frontiers in Immunology

Article Title: CRISPR/Cas9-based discovery of ccRCC therapeutic opportunities through molecular mechanism and immune microenvironment analysis

doi: 10.3389/fimmu.2025.1619361

Figure Lengend Snippet: Correlation of immune microenvironment with risk score. (A) Immune cell infiltration landscape in ccRCC revealed by CIBERSORT. (B–F) Linear regression models demonstrate risk score-dependent immune cell infiltration patterns. (G) Differential immune cell distribution between risk groups. (H–J) Risk-stratified therapeutic sensitivity to pazopanib, sunitinib, and temsirolimus.

Article Snippet: The ccRCC cell lines 786O, 769P, and Caki-1 were obtained from the American Type Culture Collection (ATCC).

Techniques:

MELK is a poor prognostic marker in ccRCC. (A) Significant variations in overall survival between ccRCC patients with high and low MELK expression. (B, C) Immunohistochemical evidence of MELK overexpression in tumor tissues versus NAT. (D) Successful MELK knockdown confirmed by western blot across 769P, 786O and Caki-1 cell lines. (E) Silencing MELK suppressed proliferation abilities in 769P, 786O and Caki-1 cells. (F–I) Silencing MELK suppressed migration abilities as measured via transwell assay (F) and scratch assay (G–I) in 769P, 786O and Caki-1 cells. * p < 0.05; ** p < 0.01; *** p < 0.001.

Journal: Frontiers in Immunology

Article Title: CRISPR/Cas9-based discovery of ccRCC therapeutic opportunities through molecular mechanism and immune microenvironment analysis

doi: 10.3389/fimmu.2025.1619361

Figure Lengend Snippet: MELK is a poor prognostic marker in ccRCC. (A) Significant variations in overall survival between ccRCC patients with high and low MELK expression. (B, C) Immunohistochemical evidence of MELK overexpression in tumor tissues versus NAT. (D) Successful MELK knockdown confirmed by western blot across 769P, 786O and Caki-1 cell lines. (E) Silencing MELK suppressed proliferation abilities in 769P, 786O and Caki-1 cells. (F–I) Silencing MELK suppressed migration abilities as measured via transwell assay (F) and scratch assay (G–I) in 769P, 786O and Caki-1 cells. * p < 0.05; ** p < 0.01; *** p < 0.001.

Article Snippet: The ccRCC cell lines 786O, 769P, and Caki-1 were obtained from the American Type Culture Collection (ATCC).

Techniques: Marker, Expressing, Immunohistochemical staining, Over Expression, Knockdown, Western Blot, Migration, Transwell Assay, Wound Healing Assay

The role of SLC6A19 in ccRCC; (A) Univariate Cox regression for SLC6A19, SLC6A12 and SMIM24. (B) Differential expression of SLC6A19 between tumor and normal tissues in TCGA,GSE53757; (C) Differential expression of SLC6A19 in various clinical stages; (D) Immunohistochemical result from the HPA database showing SLC6A19 expression in normal tissue; (E) Immunohistochemical result from the HPA database showing SLC6A19 expression in ccRCC tissue; (F) Transwell assay showing the impact of SLC6A19 to invasive ability of 786O and A498 cell lines; (G) CCK8 assay showing the impact of SLC6A19 to proliferation of 786O and A498 cell lines. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.001. ns, not significant.

Journal: Frontiers in Endocrinology

Article Title: Identification of a novel prognostic and therapeutic prediction model in clear cell renal carcinoma based on Renin-angiotensin system related genes

doi: 10.3389/fendo.2025.1521940

Figure Lengend Snippet: The role of SLC6A19 in ccRCC; (A) Univariate Cox regression for SLC6A19, SLC6A12 and SMIM24. (B) Differential expression of SLC6A19 between tumor and normal tissues in TCGA,GSE53757; (C) Differential expression of SLC6A19 in various clinical stages; (D) Immunohistochemical result from the HPA database showing SLC6A19 expression in normal tissue; (E) Immunohistochemical result from the HPA database showing SLC6A19 expression in ccRCC tissue; (F) Transwell assay showing the impact of SLC6A19 to invasive ability of 786O and A498 cell lines; (G) CCK8 assay showing the impact of SLC6A19 to proliferation of 786O and A498 cell lines. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.001. ns, not significant.

Article Snippet: The 786O and A498 cancer cell lines were purchased from CellSource China.

Techniques: Quantitative Proteomics, Immunohistochemical staining, Expressing, Transwell Assay, CCK-8 Assay

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1) Product Images from "Integrated spatial and single‑cell transcriptomics maps disulfidptosis in renal cell carcinoma and reveals PDLIM1 as a prognostic biomarker and potential therapeutic target"

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