blca cells human blca cell lines  (ATCC)

Journal: Journal of Translational Medicine

Article Title: Glutamine metabolism reprogramming promotes bladder cancer progression via PYCR1: a multi-omics and functional validation study

doi: 10.1186/s12967-025-07386-2

Figure Lengend Snippet: Glutamine metabolism profiling and single-cell landscape in bladder cancer. ( A ) Schematic of targeted metabolomics workflow comparing BLCA tumor cells and normal urothelial cells. ( B ) Boxplot showing differential amino acid expression between tumor and normal cell lines. ( C ) UMAP clustering of single-cell transcriptomes from BLCA tissue samples. ( D ) Cell type annotation based on canonical markers. ( E ) Differential gene expression analysis (DEGs) across cell clusters. ( F ) Glutamine metabolism module score visualized by UMAP. ( G ) Urothelial cells colored by high/low glutamine score group. ( H ) Volcano plot of DEGs between high- and low-score groups. ( I ) GO enrichment analysis of DEGs showing involvement in metabolic and apoptotic pathways. Error bars indicate mean ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001

Article Snippet: Human BLCA cell lines (T24, J82, UMUC3, SW780) and a normal urothelial cell line (SV-HUC-1) were obtained from American Type Culture Collection (ATCC).

Techniques: Expressing, Gene Expression

Journal: Journal of Translational Medicine

Article Title: Glutamine metabolism reprogramming promotes bladder cancer progression via PYCR1: a multi-omics and functional validation study

doi: 10.1186/s12967-025-07386-2

Figure Lengend Snippet: Knockdown or inhibition of PYCR1 suppresses proliferation, migration, and tumor growth of BLCA cells in vitro and in vivo. ( A ) Western blot showing PYCR1 expression levels in BLCA cell lines and normal urothelial cell line SV-HUC-1. ( B ) Validation of PYCR1 knockdown efficiency in T24 and J82 cells using three different shRNAs. ( C ) CCK-8 assay showing reduced proliferation of T24 and J82 cells upon PYCR1 knockdown. ( D ) Colony formation assay indicating a significant decrease in clonogenic ability after PYCR1 knockdown. ( E ) Transwell migration assay demonstrating impaired migration in PYCR1 knockdown cells, scale bar = 200 μm. ( F ) Flow cytometry analysis of cell cycle distribution in J82 and T24 cells after PYCR1 knockdown. The G2 phase showed significant accumulation with P = 0.0036 for J82 cells and P = 0.0055 for T24 cells. ( G ) Flow cytometry analysis of apoptosis in T24 and J82 cells following PYCR1 knockdown. ( H ) Schematic diagram of xenograft mouse models used to evaluate the effects of PYCR1 inhibition in vivo ( n = 6 mice per group). ( I ) Tumor volume comparison and IHC staining (H&E, PYCR1, Ki-67) of xenografts from T24 cells treated with PYCR1 inhibitor versus DMSO control. ( J ) Tumor volume comparison and IHC staining of xenografts from T24-NC and T24-shPYCR1 cells. Data are presented as mean ± SD from three independent experiments. ns indicates P > 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: Human BLCA cell lines (T24, J82, UMUC3, SW780) and a normal urothelial cell line (SV-HUC-1) were obtained from American Type Culture Collection (ATCC).

Techniques: Knockdown, Inhibition, Migration, In Vitro, In Vivo, Western Blot, Expressing, Biomarker Discovery, CCK-8 Assay, Colony Assay, Transwell Migration Assay, Flow Cytometry, Comparison, Immunohistochemistry, Control

Journal: Journal of Translational Medicine

Article Title: Glutamine metabolism reprogramming promotes bladder cancer progression via PYCR1: a multi-omics and functional validation study

doi: 10.1186/s12967-025-07386-2

Figure Lengend Snippet: PYCR1 knockdown impairs proline synthesis and suppresses the PI3K/AKT/mTOR signaling pathway in BLCA cells. ( A ) Quantification of intracellular proline levels in T24 and J82 cells after PYCR1 knockdown. ( B ) Correlation analysis showing positive associations between PYCR1 expression and SLC1A5 (left) and P5CS (right) in BLCA samples. ( C ) Western blot analysis confirming that knockdown of PYCR1 reduces protein expression levels of P5CS and SLC1A5. ( D ) Heatmap of differentially expressed genes in BLCA cells following PYCR1 knockdown from RNA-seq data. ( E - F ) Pathway enrichment analyses of downregulated ( E ) and upregulated ( F ) genes after PYCR1 knockdown, indicating involvement in PI3K-AKT and immune-related signaling pathways. ( G ) Western blot analysis validating the downregulation of PI3K, AKT, and mTOR pathway components upon PYCR1 knockdown in T24 and J82 cells. ( H ) Western blot analysis of PI3K/AKT/mTOR pathway activation following PYCR1 overexpression with or without LY294002 treatment in T24 and J82 cells. PYCR1 overexpression increased phosphorylation of PI3K, AKT, and mTOR, which was reversed by the PI3K inhibitor. Vinculin served as the loading control. Data are presented as mean ± SD from three independent experiments. * P < 0.05, ** P < 0.01; oe: Overexpression

Article Snippet: Human BLCA cell lines (T24, J82, UMUC3, SW780) and a normal urothelial cell line (SV-HUC-1) were obtained from American Type Culture Collection (ATCC).

Techniques: Knockdown, Expressing, Western Blot, RNA Sequencing, Protein-Protein interactions, Activation Assay, Over Expression, Phospho-proteomics, Control