Review

786o cancer cell line (Cell Source Ltd)

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Cell Source Ltd 786o cancer cell line

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 <t>A498</t> 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.

786o Cancer Cell Line, supplied by Cell Source Ltd, 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/result/786o cancer cell line/product/Cell Source Ltd
Average 90 stars, based on 1 article reviews

786o cancer cell line - by Bioz Stars, 2026-04

90/100 stars

Images

1) Product Images from "Identification of a novel prognostic and therapeutic prediction model in clear cell renal carcinoma based on Renin-angiotensin system related genes"

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

Journal: Frontiers in Endocrinology

doi: 10.3389/fendo.2025.1521940

Figure Legend 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.

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

Image Search Results

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

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

PBMCs from ccRCC patients confer resistance to cabozantinib treatment. (A–E) Schematic of the experimental set-up. microDUO, high throughput 384-well open microchannel multi-culture plates (Onexio Biosystems) were used to determine the effect of ccRCC PBMCs on angiogenesis. (F) The total length of the endothelial tubes was normalized to EC + DMSO-only control condition (dotted line).

Journal: Integrative Biology

Article Title: Immune cell mediated cabozantinib resistance for patients with renal cell carcinoma

doi: 10.1093/intbio/zyab018

Figure Lengend Snippet: PBMCs from ccRCC patients confer resistance to cabozantinib treatment. (A–E) Schematic of the experimental set-up. microDUO, high throughput 384-well open microchannel multi-culture plates (Onexio Biosystems) were used to determine the effect of ccRCC PBMCs on angiogenesis. (F) The total length of the endothelial tubes was normalized to EC + DMSO-only control condition (dotted line).

Article Snippet: 786O ccRCC cancer cell line was purchased from ATCC (ATCC, Cat. CRL-1932TM) and were cultured in RPMI-1640 (ThermoFisher Scientific, Cat. 11875119) media supplemented with 10% fetal bovine serum (VWR) and 100 U/ml penicillin/streptomycin (ThermoFisher Scientific).

Techniques: High Throughput Screening Assay, Control

PBMCs from patients with ccRCC upregulated secretion of pro-angiogenic factors in response to cabozantinib treatment. (A) The concentration of pro-angiogenic factors was quantified using a multiplex magnetic bead-based assay (R&D Systems). The heatmap was used to visualize the differential regulation of pro-angiogenic factors in response to cabozantinib treatment in the absence and presence of cancer cells and ccRCC PBMCs. (B) The concentration of pro-angiogenic cytokines and growth factors obtained from conditioned media from mono-culture, co-culture, and tri-culture conditions treated with cabozantinib. Bars represent average ± SD of n = 3 wells for EC + DMSO, EC + cabozantinib, EC + 786O + cabozantinib, and n = 9 wells (three wells per patient, three patients in total) ( * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.005, and # P ≤ 0.0001).

Journal: Integrative Biology

Article Title: Immune cell mediated cabozantinib resistance for patients with renal cell carcinoma

doi: 10.1093/intbio/zyab018

Figure Lengend Snippet: PBMCs from patients with ccRCC upregulated secretion of pro-angiogenic factors in response to cabozantinib treatment. (A) The concentration of pro-angiogenic factors was quantified using a multiplex magnetic bead-based assay (R&D Systems). The heatmap was used to visualize the differential regulation of pro-angiogenic factors in response to cabozantinib treatment in the absence and presence of cancer cells and ccRCC PBMCs. (B) The concentration of pro-angiogenic cytokines and growth factors obtained from conditioned media from mono-culture, co-culture, and tri-culture conditions treated with cabozantinib. Bars represent average ± SD of n = 3 wells for EC + DMSO, EC + cabozantinib, EC + 786O + cabozantinib, and n = 9 wells (three wells per patient, three patients in total) ( * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.005, and # P ≤ 0.0001).

Techniques: Concentration Assay, Multiplex Assay, Bead-based Assay, Co-Culture Assay

PLSR analysis of MDSC and T cell subsets and cabozantinib resistance. PBMCs isolated from nine patients with ccRCC undergoing systemic therapy were profiled for MDSC and T cell subtypes using flow cytometry. A PLSR model was generated using flow cytometry data as independent variables and cabozantinib resistance quantified by total tube length from tri-culture angiogenesis assay as a dependent variable. (A) Scores plot separated patients according to the degree of resistance measured in the tri-culture model along the principal component 1 (PC1). (B) Loadings plot shows covariance among the immune cell subtypes with the cabozantinib resistance. (C) VIP of immune cell subtypes with VIP score >1. (D) Changes in Th9, Th17, Th22, and Th2 cells for four patients who are receiving cabozantinib treatment (solid lines) were compared to five patients who are undergoing other therapies (dotted lines, three patients for nivolumab and two patients for pazopanib). (E) Immune gene-signature analysis of 530 patients with ccRCC from TCGA cohort showed that patients with higher expressions of the Th22 gene signature had significantly better overall survival (log-rank test P = 0.027). There was no significant correlation between the Th9 gene signature and overall survival.

Journal: Integrative Biology

Article Title: Immune cell mediated cabozantinib resistance for patients with renal cell carcinoma

doi: 10.1093/intbio/zyab018

Figure Lengend Snippet: PLSR analysis of MDSC and T cell subsets and cabozantinib resistance. PBMCs isolated from nine patients with ccRCC undergoing systemic therapy were profiled for MDSC and T cell subtypes using flow cytometry. A PLSR model was generated using flow cytometry data as independent variables and cabozantinib resistance quantified by total tube length from tri-culture angiogenesis assay as a dependent variable. (A) Scores plot separated patients according to the degree of resistance measured in the tri-culture model along the principal component 1 (PC1). (B) Loadings plot shows covariance among the immune cell subtypes with the cabozantinib resistance. (C) VIP of immune cell subtypes with VIP score >1. (D) Changes in Th9, Th17, Th22, and Th2 cells for four patients who are receiving cabozantinib treatment (solid lines) were compared to five patients who are undergoing other therapies (dotted lines, three patients for nivolumab and two patients for pazopanib). (E) Immune gene-signature analysis of 530 patients with ccRCC from TCGA cohort showed that patients with higher expressions of the Th22 gene signature had significantly better overall survival (log-rank test P = 0.027). There was no significant correlation between the Th9 gene signature and overall survival.

Techniques: Isolation, Flow Cytometry, Generated, Angiogenesis Assay

Review

Structured Review

Images

1) Product Images from "Identification of a novel prognostic and therapeutic prediction model in clear cell renal carcinoma based on Renin-angiotensin system related genes"

Similar Products

Image Search Results