786o cells  (ATCC)

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

Journal: Journal of Advanced Research

Article Title: Epigenetically silenced KAT2B suppresses de novo lipogenesis through destroying HDAC5/LSD1 complex assembly in renal cell carcinoma

doi: 10.1016/j.jare.2025.08.007

Figure Lengend Snippet: KAT2B suppressed lipogenesis through FASN (A) Key rate-limiting enzymes in de novo lipogenesis and their expression levels in ccRCC and pRCC using TCGA-KIRC and TCGA-KIRP databases. Red squares and blue squares represented genes whose expression were up-regulated or down-regulated in tumors. (B) Schematic diagram for screening key lipid synthesis factors downstream of KAT2B. (C) Statistical analysis of oil red O stainging in 786O cells following knockdown of 10 key lipogenesis factors (n = 3). (D-E) Representative IHC staining for FASN in RCC cohort and statistical analysis (n = 80, paired t‐test). (F-G) After KAT2B knockdown in 786O and ACHN cells, the mRNA and protein expression of FASN was observed. (H) The cell growth curves of A498 and Caki-1 cells with KAT2B and/or FASN overexpression were determined by CCK8 assays (n = 4, independent‐samples t‐test). (I) The relative TG levels in A498 and Caki-1 cells with KAT2B and/or FASN overexpression (n = 4, independent‐samples t‐test). (J) Representative images of oil red O staining of A498 and Caki-1 cells with KAT2B and/or FASN overexpression and statistical analysis (n = 3, independent‐samples t‐test). Data were analyzed by unpaired t test (G), paired t test (E), one-way ANOVA (H, I, J) or two-way ANOVA (C).

Article Snippet: The HK‐2, 293 T, A549, PC9, T47D, MCF7, A498, Caki-1, OSRC-2, 786O, 769P and ACHN cell lines were obtained from the American Type Culture Collection (ATCC, USA) and were cultivated under proper conditions according to the manufacturer’s protocols.

Techniques: Expressing, Knockdown, Immunohistochemistry, Over Expression, Staining

Journal: Journal of Advanced Research

Article Title: Epigenetically silenced KAT2B suppresses de novo lipogenesis through destroying HDAC5/LSD1 complex assembly in renal cell carcinoma

doi: 10.1016/j.jare.2025.08.007

Figure Lengend Snippet: Hypermethylation but not VHL/HIF axis resulted in low expression of KAT2B in RCC Expression levels of HIF2a and KAT2B after hypoxia in RCC cells. (B) Expression level of KAT2B after overexpressing HIF2a in Caki-1 cells. (C) Expression level of KAT2B after overexpressing VHL in A498 cells. (D) RNA stability experiment of KAT2B in RCC and HK2 cells after treated with 20 μg/ml cycloheximide (CHX) for 0 h, 1 h, 2 h, 3 h, and 4 h and statistical diagram. (E-F) Prediction analysis of CpG islands in the sequence range of 3500 bp upstream from the transcriptional start site in the KAT2B promoter region ( http://www.urogene.org/ ). (G-H) The promoter methylation level of KAT2B in ccRCC using online database UCSC Xena ( http://xena.ucsc.edu/ ) and UALCAN ( http://ualcan.path.uab.edu/ ). (I) Scatter plot of the relationship among KAT2B expression and its promoter methylation level. (J) Representative MSP results of KAT2B methylation status in 5 paired adjacent tissues (N) and RCC tissues (T). (K-L) The mRNA and protein levels of KAT2B in RCC cell lines after 5-AZA treatment (n = 3). (M) Scatter plot of the relationship among KAT2B expression and TET1, TET2, and TET3 expression. (N) The KAT2B mRNA expression after knockdown of TET1, TET2, or TET3 in 786O cells. (O) The KAT2B protein expression after TET1 knockdown in RCC cells. Data were analyzed by one-way ANOVA (K,N) or two-way ANOVA (D).

Article Snippet: The HK‐2, 293 T, A549, PC9, T47D, MCF7, A498, Caki-1, OSRC-2, 786O, 769P and ACHN cell lines were obtained from the American Type Culture Collection (ATCC, USA) and were cultivated under proper conditions according to the manufacturer’s protocols.

Techniques: Expressing, Sequencing, Methylation, Knockdown

Journal: Journal of Advanced Research

Article Title: Epigenetically silenced KAT2B suppresses de novo lipogenesis through destroying HDAC5/LSD1 complex assembly in renal cell carcinoma

doi: 10.1016/j.jare.2025.08.007

Figure Lengend Snippet: Therapeutic targeting of KAT2B-low RCC with a FASN inhibitor (A-B) Representative images of IHC staining of FASN in RCC cohort and statistical analysis. (C) Representative images of IHC staining for FASN and KAT2B in RCC tissues with high and low KAT2B expression. (D) Scatter plot of the relationship among KAT2B expression and FASN expression in advanced RCC tumors (n = 53). (E) The cell viability of ACHN and Caki-1 cells after treated with TVB-2640 (n = 4). (F) The cell viability of 786O and 769P cells after treated with TVB-2640 (n = 10). Proteins from three independent sites in RCC tissues were extracted to detect KAT2B expression. (H) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM). 15 organoids were randomly selected from each group for statistical analysis. (I) Representative images of Caki-1 and ACHN organoids after treatment with TVB-2640 (7.5 μM) (n = 15). (J) Representative images of two PDOs with different KAT2B expression after treatment with TVB-2640 (n = 10). (K) Representative images of PRO-1 staining of PDOs. (L-M) The cell viability of ACHN cells (L) and case 1 primary RCC cells (M) with KAT2B knockdown after treated with TVB-2640 (n = 4). (N-O) The picture (N) of xenograft using 786O cells with KAT2B knockdown after treated with TVB-2640, and tumor growth curve (n = 4). Data were analyzed by unpaired t test (B, H, I, J), one-way ANOVA (O) or two-way ANOVA (E, F, G, L, M).

Article Snippet: The HK‐2, 293 T, A549, PC9, T47D, MCF7, A498, Caki-1, OSRC-2, 786O, 769P and ACHN cell lines were obtained from the American Type Culture Collection (ATCC, USA) and were cultivated under proper conditions according to the manufacturer’s protocols.

Techniques: Immunohistochemistry, Expressing, Staining, Knockdown

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

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

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

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

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