ArticleCytoJournal2025
Solute carrier family 6 member 3 promotes the development of clear cell renal cell carcinoma by enhancing glycolysis and inhibiting ferroptosis.
Article in CytoJournal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- PCK2 Inhibition Reverses Cisplatin Resistance of Non-Small Cell Lung Cancer by Triggering Ferroptosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Clear-cell renal cell carcinoma (ccRCC) is the most prevalent type of renal cancer. Solute carrier family 6 member 3 (SLC6A3) is associated with ccRCC. This research aimed to investigate the function of SLC6A3 in promoting the metabolism and development of ccRCC tumor cells. Material and Methods: SLC6A3 expression levels in ccRCC cell lines were assessed through quantitative real-time polymerase chain reaction and Western blot (WB). A stable overexpression of SLC6A3 was achieved in the 786-O cell line, and stable knockdown was established in the OS-RC-2 cell line through lentiviral transfection. Cell biological behavior was evaluated through flow cytometry, terminal deoxynucleotidyl transferase media dUTP nick end labeling staining, Cell counting kit-8 assays, and Transwell assays. Extracellular acidification rate measurements, WB, and biochemical assays were performed to detect cellular glycolysis and ferroptosis following alterations in SLC6A3 expression. The effects of SLC6A3 overexpression or knockdown on ccRCC tumor were further verified in xenograft models using nude mice. Results: SLC6A3 was elevated in various ccRCC cell lines. The 786-O cells exhibited a relatively low baseline SLC6A3 expression ( Conclusion: SLC6A3 is markedly overexpressed in ccRCC. It influences the promotion of tumor growth by enhancing glycolysis and suppressing ferroptosis. These insights highlight the potential of SLC6A3 for innovative therapeutic strategies in ccRCC management.
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