rptec tert1 cells  (ATCC)

Journal: Journal of Toxicology

Article Title: In Vitro hRPTEC TERT1 Model for Uranium‐Induced Nephrotoxicity Pathway Study

doi: 10.1155/jt/6692188

Figure Lengend Snippet: Effect of uranium on apoptosis and necrosis for hRPTEC TERT1 cells. Cells were treated with different concentrations of uranium for 48 h. Next, cell apoptosis was measured by caspase 3/7 luminescence assay and cell necrosis was measured by LDH luminescence assay. Data were expressed as a percentage of the positive control, treatment with staurosporine 10 μM over 24 h for apoptosis induction, and treatment with triton 1% for 15 min for necrosis induction. Data were expressed as mean ± SEM where n = 8 per condition. Asterisk represents a significant difference between U (VI)‐treated and untreated cells (two‐way ANOVA ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001); sharp sign represents a significant difference between U (VI)‐treated concentrations (two‐way ANOVA # p < 0.05; ## p < 0.01; ### p < 0.001).

Article Snippet: The hRPTEC TERT1 cells (ATCC, CRL‐4031) were maintained in a DMEM/F12 medium (Cytivia), supplemented with 10 ng/mL of hEGF, 0.1 mg/mL of G418, 1% ITSG, 3.5 μg/mL of ascorbic acid, and 25 ng/mL of prostaglandin E1 (ATCC).

Techniques: Luminescence Assay, Positive Control

Journal: Journal of Toxicology

Article Title: In Vitro hRPTEC TERT1 Model for Uranium‐Induced Nephrotoxicity Pathway Study

doi: 10.1155/jt/6692188

Figure Lengend Snippet: Effect of uranium on apoptosis or survival pathway for hRPTEC TERT1 cells. Cells were treated with different concentrations of uranium for 48 h. (a) Screening of gene expression implicated in apoptosis or survival pathway. Data were expressed as mean ± SEM ( n = 8 for 0, 100 and 300 μM; n = 5 for 500 μM). (b) Proteome profiler array on apoptosis or survival pathway. Results are expressed as a chemiluminescence signal ratio (treated to untreated cells) in the form of a heat map ( n = 1 per condition). Asterisk represents a significant difference between U (VI) treated and untreated cells (two‐way ANOVA ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001); sharp sign represents a significant difference between U (VI)‐treated concentrations (two‐way ANOVA # p < 0.05; ## p < 0.01; ### p < 0.001).

Article Snippet: The hRPTEC TERT1 cells (ATCC, CRL‐4031) were maintained in a DMEM/F12 medium (Cytivia), supplemented with 10 ng/mL of hEGF, 0.1 mg/mL of G418, 1% ITSG, 3.5 μg/mL of ascorbic acid, and 25 ng/mL of prostaglandin E1 (ATCC).

Techniques: Gene Expression

Journal: Journal of Toxicology

Article Title: In Vitro hRPTEC TERT1 Model for Uranium‐Induced Nephrotoxicity Pathway Study

doi: 10.1155/jt/6692188

Figure Lengend Snippet: Effect of uranium on nephrotoxicity biomarkers for hRPTEC TERT1 cells. Cells were treated with different concentrations of uranium for 48 h. (a) Gene expression of nephrotoxicity biomarkers. Data were expressed as mean ± SEM ( n = 3 per condition). (b) Proteome profiler array on nephrotoxicity. Results are expressed as a ratio of untreated to treated cells at different concentrations in the form of a heat map ( n = 1 per condition). (c) KIM1 protein assay by Milliplex (LOQ 0.05 ng.mL −1 ). Data were expressed as mean ± SD ( n = 3 per condition). (d) Collagen IV protein assay by Milliplex (LOQ 0.5 ng.mL −1 ). Data were expressed as mean ± SD ( n = 3 per condition). Asterisk represents a significant difference between U (VI)‐treated and untreated cells (two‐way ANOVA ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001).

Article Snippet: The hRPTEC TERT1 cells (ATCC, CRL‐4031) were maintained in a DMEM/F12 medium (Cytivia), supplemented with 10 ng/mL of hEGF, 0.1 mg/mL of G418, 1% ITSG, 3.5 μg/mL of ascorbic acid, and 25 ng/mL of prostaglandin E1 (ATCC).

Techniques: Gene Expression

Journal: Journal of Toxicology

Article Title: In Vitro hRPTEC TERT1 Model for Uranium‐Induced Nephrotoxicity Pathway Study

doi: 10.1155/jt/6692188

Figure Lengend Snippet: Effect of uranium on oxidative stress for hRPTEC TERT1 cells. Cells were treated with different concentrations of uranium (U (VI)) for 48 h. (a) Gene expression of antioxidant enzymes. Results are expressed as a ratio to the expression of the housekeeping gene GAPDH. Data were expressed as mean ± SEM ( n = 8 for 0, 100, and 300 μM; n = 5 for 500 μM). (b) Gene expression of targets implicated in the oxidative stress pathway. Results are expressed as a ratio to the expression of the housekeeping gene GAPDH. Data were expressed as mean ± SEM ( n = 3 per condition). (c) Proteome profiler array on oxidative stress pathway. Results are expressed as chemiluminescence signal ratio (U (VI) treated to untreated cells) in the form of a heat map ( n = 1 per condition). (d) Kinetics of reactive oxygen species production after exposure to U (VI) for 48 h ( n = 3 per condition). Asterisk represents a significant difference between U (VI)‐treated and untreated cells (two‐way ANOVA ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001); sharp sign represents a significant difference between U(VI)‐treated concentrations (two‐way ANOVA # p < 0.05; ## p < 0.01; ### p < 0.001).

Article Snippet: The hRPTEC TERT1 cells (ATCC, CRL‐4031) were maintained in a DMEM/F12 medium (Cytivia), supplemented with 10 ng/mL of hEGF, 0.1 mg/mL of G418, 1% ITSG, 3.5 μg/mL of ascorbic acid, and 25 ng/mL of prostaglandin E1 (ATCC).

Techniques: Gene Expression, Expressing

Journal: Journal of Toxicology

Article Title: In Vitro hRPTEC TERT1 Model for Uranium‐Induced Nephrotoxicity Pathway Study

doi: 10.1155/jt/6692188

Figure Lengend Snippet: Effect of uranium on inflammation for hRPTEC TERT1 cells. Cells were treated with different concentrations of uranium for 48 h. (a) Screening of gene expression implicated in the inflammation pathway. Data were expressed as mean ± SEM ( n = 3 per condition). (b) Proteome profiler array on inflammation pathway. Results are expressed as a ratio of untreated to treated cells at different concentrations in the form of a heat map ( n = 1 per condition). (c) TNFα protein assay by Milliplex. Data were expressed as mean ± SD ( n = 3 per condition). (d) IL‐6 protein assay by Milliplex. Data were expressed as mean ± SD ( n = 3 per condition). (e) IL‐18 protein assay by Milliplex. Data were expressed as mean ± SD ( n = 3 per condition). Asterisk represents a significant difference between U (VI)‐treated and untreated cells (two‐way ANOVA ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001); sharp sign represents a significant difference between U (VI)‐treated concentrations (two‐way ANOVA # p < 0.05; ## p < 0.01; ### p < 0.001).

Article Snippet: The hRPTEC TERT1 cells (ATCC, CRL‐4031) were maintained in a DMEM/F12 medium (Cytivia), supplemented with 10 ng/mL of hEGF, 0.1 mg/mL of G418, 1% ITSG, 3.5 μg/mL of ascorbic acid, and 25 ng/mL of prostaglandin E1 (ATCC).

Techniques: Gene Expression

Journal: Oncology Reports

Article Title: Mechanistic study of MUC3A in promoting progression of clear cell renal cell carcinoma via the JAK-STAT pathway

doi: 10.3892/or.2026.9119

Figure Lengend Snippet: MUC3A is aberrantly upregulated in ccRCC and associated with poor prognosis. (A) Pan-cancer analysis of MUC3A expression across multiple tumor types based on TCGA data, generated using the GEPIA2 platform. Gene expression values are presented as log2(TPM + 1). (B) Differential expression of MUC3A in tumor and normal samples from the TCGA-KIRC cohort (523 tumor samples vs. 72 normal samples). *P<0.05. (C) Western blotting of MUC3A protein expression in HK-2 and RPTEC/TERT1 non-malignant renal epithelial cell lines and ccRCC cell lines (CAKI-1, OSRC-2, 786-O and ACHN). GAPDH was used as a loading control. (D) Western blotting of MUC3A knockdown efficiency in 786-O and OSRC-2 cells following transient transfection with three independent siRNAs targeting MUC3A. si-2 was selected for subsequent functional experiments due to its superior knockdown efficiency. (E) Kaplan-Meier OS analysis of ccRCC patients stratified into high- and low-MUC3A expression groups using the GEPIA2 platform. (F) Kaplan-Meier DFS analysis of ccRCC patients based on MUC3A expression levels. Data are derived from TCGA unless otherwise indicated. MUC3A, mucin 3A; ccRCC, clear cell renal cell carcinoma; TCGA, The Cancer Genome Atlas; KIRC, kidney renal clear cell carcinoma; GEPIA2, Gene Expression Profiling Interactive Analysis 2; TPM, transcripts per million; KIRC, kidney renal clear cell carcinoma; OS, overall survival; DFS, disease-free survival; siRNA, small interfering RNA; si-MUC3A, MUC3A-targeting siRNA; si-Ctrl, non-targeting control siRNA; GAPDH, glyceraldehyde-3-phosphate dehydrogenase; si-1/si-2/si-3, three independent siRNAs targeting MUC3A.

Article Snippet: Human ccRCC cell lines 786-O (cat. no. CL-0010), OSRC-2 (cat. no. CL-0177), Caki-1 (cat. no. CL-0052) and ACHN (cat. no. CL-0021), as well as non-malignant renal epithelial cells HK-2 (cat. no. CL-0109; all from Procell Life Science & Technology Co., Ltd.) and RPTEC/TERT1 (cat. no. CRL-4031; American Type Culture Collection), were used in the present study.

Techniques: Expressing, Generated, Gene Expression, Quantitative Proteomics, Western Blot, Control, Knockdown, Transfection, Functional Assay, Derivative Assay, Small Interfering RNA