sunitinib resistant 786o cell line  (MedChemExpress)

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

Journal: Pharmaceutics

Article Title: Rational Design of Non-Toxic Multidrug Combinations Demonstrates Durable and Hypoxia-Enhanced Efficacy Against Renal Cell Carcinoma

doi: 10.3390/pharmaceutics17101269

Figure Lengend Snippet: Selectivity of the ODCs. ( A , B ) ATP levels of ( A ) 786O cells or ( B ) RPTEC cells treated with variations of the four drugs present in the third search of the 786O-based screen. ( C ) TW of each condition tested in ( A , B ) calculated for each condition as the ATP levels of ( A ) subtracted from the ATP levels of ( B , D , E ) ATP levels of ( D ) UOK276 cells or ( E ) RPTEC cells treated with the four drugs, found in the third search of the UOK276-based screen, combined or as single agents. ( F ) TW of each condition tested in ( D , E ) calculated for each condition as the ATP levels of ( D ) subtracted from the ATP levels of ( E , G , H ) ATP level of ( G ) 786O cells or ( H ) RPTEC cells treated with three drugs of the additive combination found in the 786O-based screen, either combined or as single agents. ( I ) TW of each condition tested in ( G , H ) calculated for each condition as the ATP levels of ( G ) subtracted from the ATP levels of ( H ). ( A , B , D , E , G , H ) Significance was calculated between DMSO controls and all conditions using One-way ANOVA with Dunnett’s multiple comparison test. ns p > 0.05, * p < 0.05, ** p < 0.01, and **** p < 0.0001. ( J ) Regression coefficients estimated from a computational model based on experimental data from treated 786O cells. Histograms are separated by empty ticks into three parts representing (from left to right) 1st order single drug activity, drug–drug interactions, and 2nd order single drug activity. Error bars and stars correspond to the standard deviation and significance of the regression coefficients, respectively. Screening was performed as N = 3 independent experiments. ( K ) Schematic representation of the pathways targeted by the drugs composing the selected ODCs. Created with BioRender.

Article Snippet: 786O cells (ATCC, CRL-1932) were cultivated in RPMI medium with Glutamax (ThermoFisher Scientific, Waltham, MA, USA, 61870-010) supplemented with 10% fetal bovine serum (FBS; Biowest, Nuaillé, France, S1810-500) and 1% penicillin/streptomycin (Sigma-Aldrich, Saint-Louis, MO, USA, P0781-100ML).

Techniques: Comparison, Activity Assay, Standard Deviation

Journal: Pharmaceutics

Article Title: Rational Design of Non-Toxic Multidrug Combinations Demonstrates Durable and Hypoxia-Enhanced Efficacy Against Renal Cell Carcinoma

doi: 10.3390/pharmaceutics17101269

Figure Lengend Snippet: Cross-activity and safety profiles of the ODCs. ATP levels of ( A ) 786O or ( B ) UOK276 cells after 72 h of exposure to the ODCs (light blue) or their composing monotherapies (orange). All data are shown as percentages of the 0.054% DMSO control (dark blue). Culture medium control is presented as a yellow bar. Error bars indicate the standard deviation (metabolic activity measurement, N = 3–4). Circles highlight each technical replicate (n = 2–3). Significance is calculated with One-way ANOVA with Tukey’s multiple comparisons test. ( C ) ATP level of patient-derived kidney organoids (PHK28) treated for 72 h with the ODCs (light blue), corresponding monotherapies (orange), as well as positive (pink) and negative controls (dark blue and yellow). ( D ) ATP level of H9c2 cells differentiated for two weeks with 1 μM all-trans retinoic acid then treated for 72 h with the ODCs (light blue), corresponding monotherapies (orange), as well as positive (pink) and negative controls (dark blue and yellow). ( E , F ) ATP level of differentiated HepaRG cells treated for 72 h ( E ) in 2D or ( F ) in 3D with the ODCs (light blue), corresponding monotherapies (orange), as well as positive (pink) and negative controls (dark blue and yellow). ( C – F ) All results except ( C ) cisplatin and 0.1% DMF conditions are displayed as a percentage of the 0.1% DMSO control (dark blue). Cisplatin (pink) and 0.1% DMF (grey) conditions are shown as percentages of the 0.1% DMF condition. Significance was calculated with One-way ANOVA with Šídák’s multiple comparisons test. ( A – F ) Only comparisons to the DMSO controls, comparisons in-between ODCs, and comparisons between ODCs and their composing monotherapies were kept on the graphs. Significance is displayed as and displayed as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. The absence of asterisk between mentioned conditions means non-significant differences ( p > 0.05).

Article Snippet: 786O cells (ATCC, CRL-1932) were cultivated in RPMI medium with Glutamax (ThermoFisher Scientific, Waltham, MA, USA, 61870-010) supplemented with 10% fetal bovine serum (FBS; Biowest, Nuaillé, France, S1810-500) and 1% penicillin/streptomycin (Sigma-Aldrich, Saint-Louis, MO, USA, P0781-100ML).

Techniques: Activity Assay, Control, Standard Deviation, Derivative Assay

Journal: Pharmaceutics

Article Title: Rational Design of Non-Toxic Multidrug Combinations Demonstrates Durable and Hypoxia-Enhanced Efficacy Against Renal Cell Carcinoma

doi: 10.3390/pharmaceutics17101269

Figure Lengend Snippet: Effect of oxygen and culture dimension on ODCs’ activity. ( A ) Schematic drawing of the different culture/treatment conditions tested in ( B – G ). Created with BioRender. ( B , C ) ATP levels of ( B ) 786O or ( C ) UOK276 cells cultivated as 2D monolayers in a 1.5% oxygen environment and exposed for 72 h to the ODCs (light blue) or their composing monotherapies (orange). ( D , F ) ATP levels of ( D ) 786O and ( F ) UOK276 spheroids cultivated in atmospheric normoxia and exposed for 72 h to the ODCs (light blue) or their composing monotherapies (orange). ( E , G ) ATP levels of ( E ) 786O and ( G ) UOK276 spheroids cultivated in a 1.5% oxygen environment and exposed for 72 h to the ODCs (light blue) or their composing monotherapies (orange). ( B – G ) All data are shown as percentages of the 0.054% DMSO controls (dark blue). Culture medium control is presented as a yellow bar. Error bars indicate the standard deviation (metabolic activity measurement, N = 3) Circles highlight each technical replicate (n = 2–3). Significance was calculated using One-way ANOVA with Šídák’s multiple comparisons test and displayed as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. Only comparisons to the DMSO controls, comparisons in-between ODCs, and comparisons between ODCs and their composing monotherapies were kept on the graphs. The absence of an asterisk between mentioned conditions means non-significant differences ( p > 0.05).

Article Snippet: 786O cells (ATCC, CRL-1932) were cultivated in RPMI medium with Glutamax (ThermoFisher Scientific, Waltham, MA, USA, 61870-010) supplemented with 10% fetal bovine serum (FBS; Biowest, Nuaillé, France, S1810-500) and 1% penicillin/streptomycin (Sigma-Aldrich, Saint-Louis, MO, USA, P0781-100ML).

Techniques: Activity Assay, Control, Standard Deviation

Journal: Pharmaceutics

Article Title: Rational Design of Non-Toxic Multidrug Combinations Demonstrates Durable and Hypoxia-Enhanced Efficacy Against Renal Cell Carcinoma

doi: 10.3390/pharmaceutics17101269

Figure Lengend Snippet: Effect of repeated exposure on treatment response. ( A , C , D ) Schematic representation of the different re-treatment strategies adopted for retreatment of ( A ) the same plate, ( C ) the same cell population, and ( D ) of the same cell population for a long period. ( B ) Response to first (orange) and second (red) treatment in 786O (top) and UOK276 (bottom) following the method described in ( A ). Each cell line was treated only with the ODC(s) and corresponding monotherapies identified in that same cell line. Both graphs are the results of N = 3 independent experiments including n = 3 technical replicate for each condition. ( C ) Data generated following this protocol can be found in . ( E ) Results of the retreatment with ODC conducted as indicated in ( D ) on 786O (left) and UOK276 (right) cells. Each point in the graphs corresponds to the mean of three measurement from N = 1 independent experiment. Color code can be found in the legend (far right) and is valid for both cell lines. Graduation on the x -axis corresponds to the number of times the cells were exposed to the drugs for 72 h. Circles highlight each technical replicate (n = 3). Significance was calculated using Two-way ANOVA with Šídák’s multiple comparisons test and displayed as * p < 0.05, ** p < 0.01, and **** p < 0.0001.

Article Snippet: 786O cells (ATCC, CRL-1932) were cultivated in RPMI medium with Glutamax (ThermoFisher Scientific, Waltham, MA, USA, 61870-010) supplemented with 10% fetal bovine serum (FBS; Biowest, Nuaillé, France, S1810-500) and 1% penicillin/streptomycin (Sigma-Aldrich, Saint-Louis, MO, USA, P0781-100ML).

Techniques: Generated

Journal: Pharmaceutics

Article Title: Rational Design of Non-Toxic Multidrug Combinations Demonstrates Durable and Hypoxia-Enhanced Efficacy Against Renal Cell Carcinoma

doi: 10.3390/pharmaceutics17101269

Figure Lengend Snippet: Insight into the mechanism of the ODCs. Percentage of counted living cells in treated ( A ) 786O and ( B ) UOK276 cells compared to the count in the 0.054% DMSO control. ( C , D ) Percentage of dead cells compared to the total cell count in each treated condition for ( C ) 786O-treated flasks and ( D ) UOK276-treated flasks. ( A – D ) Error bars indicate the standard deviation (cell count measurement of N = 3 independent experiments). Circles highlight each technical replicate (n = 1). Significance was calculated using Two-way ANOVA with Tukey’s multiple comparisons test and displayed as * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. ( E ) Cell cycle distribution of 786O (top) and UOK276 (bottom) cells exposed for 24 h to the ODCs or controls. The cell cycle phases color code in both graphs is as indicated in the legend (middle). Significance was calculated between similar cell cycle phases of all conditions using Two-way ANOVA with Tukey’s multiple comparisons test and displayed as * p < 0.05, ** p < 0.01, and *** p < 0.001. Examples of the gating can be found in . ( F ) Venn diagram of genes significantly affected by ODC A (A), ODC B (B), and/or ODC C (C) in 786O (left) and UOK276 (right) cells. ( G ) Heatmaps of up- (red) and down- (blue) regulated genes in 786O (left) and UOK276 (right) cells after 72 h of treatment with the ODCs. “NEV” (center) stands for Normalized Expression Values. ( F , G ) Only the genes that are significantly different ( p < 0.05) and have a fold change superior to or equal to 2 compared to the 0.054% DMSO control are displayed.

Article Snippet: 786O cells (ATCC, CRL-1932) were cultivated in RPMI medium with Glutamax (ThermoFisher Scientific, Waltham, MA, USA, 61870-010) supplemented with 10% fetal bovine serum (FBS; Biowest, Nuaillé, France, S1810-500) and 1% penicillin/streptomycin (Sigma-Aldrich, Saint-Louis, MO, USA, P0781-100ML).

Techniques: Control, Cell Counting, Standard Deviation, Expressing

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

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

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:

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:

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

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