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cell culture renal cancer cell lines 786 o (ATCC)

Name: cell culture renal cancer cell lines 786 o
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Rating: 99 (2340 reviews)

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ATCC cell culture renal cancer cell lines 786 o
Cell Culture Renal Cancer Cell Lines 786 O, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 2340 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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cell culture renal cancer cell lines 786 o - by Bioz Stars, 2026-02

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NUMBL promotes migration, invasion, and proliferation of ccRCC cells. A , the expression level of NUMBL in all RCCs in the CCLE database. B and C , detecting the differential expression of NUMBL between ccRCC cells and renal tubular epithelial cells (HK2) using WB. D and E , knockdown of NUMBL in OSRC2 and 769P. F , overexpression of NUMBL in ACHN. G – I , the migration abilities of OSRC2, 769P, and ACHN were evaluated using a wound healing assay following NUMBL expression interference. J – L , the migration and invasion abilities of OSRC2, 769P, and ACHN cells were assessed using Transwell assays with interferencing NUMBL expression. M – O , proliferation was assessed using colony formation assays. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. ccRCC, clear cell renal cell carcinoma; CCLE, Cancer Cell Line Encyclopedia; NUMBL, NUMB-like endocytic adaptor protein; WB, Western blot.

Journal: The Journal of Biological Chemistry

Article Title: Mechanism of NUMBL enhancing axitinib resistance in clear cell renal cell carcinoma by UCHL1-mediated deubiquitination of MMP9

doi: 10.1016/j.jbc.2025.110873

Figure Lengend Snippet: NUMBL promotes migration, invasion, and proliferation of ccRCC cells. A , the expression level of NUMBL in all RCCs in the CCLE database. B and C , detecting the differential expression of NUMBL between ccRCC cells and renal tubular epithelial cells (HK2) using WB. D and E , knockdown of NUMBL in OSRC2 and 769P. F , overexpression of NUMBL in ACHN. G – I , the migration abilities of OSRC2, 769P, and ACHN were evaluated using a wound healing assay following NUMBL expression interference. J – L , the migration and invasion abilities of OSRC2, 769P, and ACHN cells were assessed using Transwell assays with interferencing NUMBL expression. M – O , proliferation was assessed using colony formation assays. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. ccRCC, clear cell renal cell carcinoma; CCLE, Cancer Cell Line Encyclopedia; NUMBL, NUMB-like endocytic adaptor protein; WB, Western blot.

Article Snippet: The human renal cancer cell lines 769P, OSRC2, and ACHN (obtained from the American Type Culture Collection) were cultured using standard methods.

Techniques: Migration, Expressing, Quantitative Proteomics, Knockdown, Over Expression, Wound Healing Assay, Western Blot

NUMBL promotes VM in ccRCC cells. A , VM (PAS+/CD31-) exists in ccRCC tissues. B , tube formation assay detects VM in OSRC2, 769P, and ACHN. C – H , based on , D – F , the VM capacity of ccRCC cells was assessed using tube formation assays. I – K , based on , D – F , the drug sensitivity of ccRCC cells to axitinib was evaluated using CCK-8 assays. CCK-8, Cell Counting Kit-8; ccRCC, clear cell renal cell carcinoma; NUMBL, NUMB-like endocytic adaptor protein; PAS, Periodic Acid-Schiff; VM, vasculogenic mimicry.

Journal: The Journal of Biological Chemistry

Article Title: Mechanism of NUMBL enhancing axitinib resistance in clear cell renal cell carcinoma by UCHL1-mediated deubiquitination of MMP9

doi: 10.1016/j.jbc.2025.110873

Figure Lengend Snippet: NUMBL promotes VM in ccRCC cells. A , VM (PAS+/CD31-) exists in ccRCC tissues. B , tube formation assay detects VM in OSRC2, 769P, and ACHN. C – H , based on , D – F , the VM capacity of ccRCC cells was assessed using tube formation assays. I – K , based on , D – F , the drug sensitivity of ccRCC cells to axitinib was evaluated using CCK-8 assays. CCK-8, Cell Counting Kit-8; ccRCC, clear cell renal cell carcinoma; NUMBL, NUMB-like endocytic adaptor protein; PAS, Periodic Acid-Schiff; VM, vasculogenic mimicry.

Article Snippet: The human renal cancer cell lines 769P, OSRC2, and ACHN (obtained from the American Type Culture Collection) were cultured using standard methods.

Techniques: Tube Formation Assay, CCK-8 Assay, Cell Counting

Upregulated NUMBL enhances the mRNA stability of UCHL1. A , transcriptome sequencing following NUMBL knockdown in 769P cells. B , proteome sequencing after NUMBL knockdown in 769P cells. C and D , validate the mRNA changes of UCHL1 after interfering with NUMBL expression in 769P and ACHN cells. E – F , confirm via WB that UCHL1 protein levels change with NUMBL expression after NUMBL interference in 769P and ACHN cells. G , the correlation between NUMBL and UCHL1 in the TCGA database. H , the correlation between NUMBL and UCHL1 in the CPTAC database. I , based on the treatment in D , after treating 769P cells with stable NUMBL knockdown with actinomycin D , UCHL1 mRNA levels were measured at specific time points. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. CPTAC, Clinical Proteomic Tumor Analysis Consortium; NUMBL, NUMB-like endocytic adaptor protein; TCGA, The Cancer Genome Atlas; UCHL1, ubiquitin C-terminal hydrolase L1; WB, Western blot.

Journal: The Journal of Biological Chemistry

Article Title: Mechanism of NUMBL enhancing axitinib resistance in clear cell renal cell carcinoma by UCHL1-mediated deubiquitination of MMP9

doi: 10.1016/j.jbc.2025.110873

Figure Lengend Snippet: Upregulated NUMBL enhances the mRNA stability of UCHL1. A , transcriptome sequencing following NUMBL knockdown in 769P cells. B , proteome sequencing after NUMBL knockdown in 769P cells. C and D , validate the mRNA changes of UCHL1 after interfering with NUMBL expression in 769P and ACHN cells. E – F , confirm via WB that UCHL1 protein levels change with NUMBL expression after NUMBL interference in 769P and ACHN cells. G , the correlation between NUMBL and UCHL1 in the TCGA database. H , the correlation between NUMBL and UCHL1 in the CPTAC database. I , based on the treatment in D , after treating 769P cells with stable NUMBL knockdown with actinomycin D , UCHL1 mRNA levels were measured at specific time points. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. CPTAC, Clinical Proteomic Tumor Analysis Consortium; NUMBL, NUMB-like endocytic adaptor protein; TCGA, The Cancer Genome Atlas; UCHL1, ubiquitin C-terminal hydrolase L1; WB, Western blot.

Article Snippet: The human renal cancer cell lines 769P, OSRC2, and ACHN (obtained from the American Type Culture Collection) were cultured using standard methods.

Techniques: Sequencing, Knockdown, Expressing, Ubiquitin Proteomics, Western Blot

UCHL1 stabilizes the expression of MMP9 protein. A , heatmap of the correlation between NUMBL and the VM gene set. B , identify the intersection between the ECM gene set and the VM gene set. C – F , correlation analysis of the four genes in the intersection with UCHL1 in the CPTAC database. G – H , knocking down NUMBL in 769P cells results in decreased expression of MMP9. I – J , treating 769P cells with 20 μM of MG-132 for 12 h results in increased expression of MMP9. K , the co-IP experiment detects an interaction between MMP9 and UCHL1. L , MMP9 undergoes ubiquitination modification. M and P , WB is used to detect the efficiency of knocking down UCHL1. N , knocking down UCHL1 in 769P cells results in increased ubiquitination levels of MMP9. O , immunofluorescence staining reveals colocalization of UCHL1 and MMP9 in the cytoplasm of 769P cells. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. co-IP, coimmunoprecipitation; CPTAC, Clinical Proteomic Tumor Analysis Consortium; ECM, extracellular matrix; MMP9, matrix metalloproteinase 9; UCHL1, ubiquitin C-terminal hydrolase L1; VM, vasculogenic mimicry; WB, Western blot.

Journal: The Journal of Biological Chemistry

Article Title: Mechanism of NUMBL enhancing axitinib resistance in clear cell renal cell carcinoma by UCHL1-mediated deubiquitination of MMP9

doi: 10.1016/j.jbc.2025.110873

Figure Lengend Snippet: UCHL1 stabilizes the expression of MMP9 protein. A , heatmap of the correlation between NUMBL and the VM gene set. B , identify the intersection between the ECM gene set and the VM gene set. C – F , correlation analysis of the four genes in the intersection with UCHL1 in the CPTAC database. G – H , knocking down NUMBL in 769P cells results in decreased expression of MMP9. I – J , treating 769P cells with 20 μM of MG-132 for 12 h results in increased expression of MMP9. K , the co-IP experiment detects an interaction between MMP9 and UCHL1. L , MMP9 undergoes ubiquitination modification. M and P , WB is used to detect the efficiency of knocking down UCHL1. N , knocking down UCHL1 in 769P cells results in increased ubiquitination levels of MMP9. O , immunofluorescence staining reveals colocalization of UCHL1 and MMP9 in the cytoplasm of 769P cells. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. co-IP, coimmunoprecipitation; CPTAC, Clinical Proteomic Tumor Analysis Consortium; ECM, extracellular matrix; MMP9, matrix metalloproteinase 9; UCHL1, ubiquitin C-terminal hydrolase L1; VM, vasculogenic mimicry; WB, Western blot.

Article Snippet: The human renal cancer cell lines 769P, OSRC2, and ACHN (obtained from the American Type Culture Collection) were cultured using standard methods.

Techniques: Expressing, Co-Immunoprecipitation Assay, Ubiquitin Proteomics, Modification, Immunofluorescence, Staining, Western Blot

The NUMBL–UCHL1–MMP9 pathway is involved in the development of ccRCC in vivo . A , photographs of tumors at the final time point (15 days after subcutaneous transplantation of 769P cells). B and C , tumor volumes and weights were measured following resection in each group. D and E , immunohistochemical staining was used to detect MMP9 and Ki-67 expression in tumor tissues. F , immunofluorescence staining is used to examine the expression of Ki-67 in tumor tissues. The scale bar represents 100 μm. Original magnification, 200×. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. ccRCC, clear cell renal cell carcinoma; MMP9, matrix metalloproteinase 9; NUMBL, NUMB-like endocytic adaptor protein; UCHL1, ubiquitin C-terminal hydrolase L1.

Journal: The Journal of Biological Chemistry

Article Title: Mechanism of NUMBL enhancing axitinib resistance in clear cell renal cell carcinoma by UCHL1-mediated deubiquitination of MMP9

doi: 10.1016/j.jbc.2025.110873

Figure Lengend Snippet: The NUMBL–UCHL1–MMP9 pathway is involved in the development of ccRCC in vivo . A , photographs of tumors at the final time point (15 days after subcutaneous transplantation of 769P cells). B and C , tumor volumes and weights were measured following resection in each group. D and E , immunohistochemical staining was used to detect MMP9 and Ki-67 expression in tumor tissues. F , immunofluorescence staining is used to examine the expression of Ki-67 in tumor tissues. The scale bar represents 100 μm. Original magnification, 200×. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. ccRCC, clear cell renal cell carcinoma; MMP9, matrix metalloproteinase 9; NUMBL, NUMB-like endocytic adaptor protein; UCHL1, ubiquitin C-terminal hydrolase L1.

Article Snippet: The human renal cancer cell lines 769P, OSRC2, and ACHN (obtained from the American Type Culture Collection) were cultured using standard methods.

Techniques: In Vivo, Transplantation Assay, Immunohistochemical staining, Staining, Expressing, Immunofluorescence, Ubiquitin Proteomics

Inhibiting the expression of NUMBL enhances the sensitivity of 769P R to axitinib. A , using the CCK-8 assay to verify the standardization of drug-resistant strain construction (DRI = 9.75). B and C , WB analysis was conducted to detect changes in NUMBL expression levels between 769P R and 769P. D and E , WB analysis was performed to detect the knockdown of NUMBL in 769P R cells. F and G , proliferation was assessed using colony formation assays. H , tube formation assay was conducted to detect the tubulogenesis ability of 769P R cells after NUMBL knockdown. I – L , based on D , a wound healing assay was performed to detect the migration ability of 769P R cells after NUMBL knockdown, whereas a Transwell assay was conducted to assess both migration and invasion capabilities. M , a CCK-8 assay was conducted to detect the sensitivity of 769P R cells to axitinib after NUMBL knockdown. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. CCK-8, Cell Counting Kit-8; DRI, drug resistance index; NUMBL, NUMB-like endocytic adaptor protein; WB, Western blot.

Journal: The Journal of Biological Chemistry

Article Title: Mechanism of NUMBL enhancing axitinib resistance in clear cell renal cell carcinoma by UCHL1-mediated deubiquitination of MMP9

doi: 10.1016/j.jbc.2025.110873

Figure Lengend Snippet: Inhibiting the expression of NUMBL enhances the sensitivity of 769P R to axitinib. A , using the CCK-8 assay to verify the standardization of drug-resistant strain construction (DRI = 9.75). B and C , WB analysis was conducted to detect changes in NUMBL expression levels between 769P R and 769P. D and E , WB analysis was performed to detect the knockdown of NUMBL in 769P R cells. F and G , proliferation was assessed using colony formation assays. H , tube formation assay was conducted to detect the tubulogenesis ability of 769P R cells after NUMBL knockdown. I – L , based on D , a wound healing assay was performed to detect the migration ability of 769P R cells after NUMBL knockdown, whereas a Transwell assay was conducted to assess both migration and invasion capabilities. M , a CCK-8 assay was conducted to detect the sensitivity of 769P R cells to axitinib after NUMBL knockdown. Data were shown as mean ± SD of at least three independent experiments for every cell line. Statistical differences were determined using Tukey's post hoc one-way ANOVA test. NS, nonstatistically significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. CCK-8, Cell Counting Kit-8; DRI, drug resistance index; NUMBL, NUMB-like endocytic adaptor protein; WB, Western blot.

Article Snippet: The human renal cancer cell lines 769P, OSRC2, and ACHN (obtained from the American Type Culture Collection) were cultured using standard methods.

Techniques: Expressing, CCK-8 Assay, Knockdown, Tube Formation Assay, Wound Healing Assay, Migration, Transwell Assay, Cell Counting, Western Blot

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

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