ArticleJournal of gastrointestinal oncology2025
ZNF454-FSTL3 axis inhibits colorectal cancer progression by inhibiting HIF-1α-mediated glycolysis in hypoxia.
Article in Journal of gastrointestinal oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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6 authors.
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Abstract
Background: Our preliminary experiments confirmed that follistatin-like 3 (FSTL3) expression is elevated in colorectal cancer (CRC) cells following CoCl Methods: CoCl Results: We found that both FSTL3 and hypoxia-inducible factor 1α (HIF-1α) were upregulated in CRC tissues and in CRC cells under hypoxic conditions, with a positive correlation between their expression in clinical samples. Silencing FSTL3 reduced HIF-1α expression and suppressed the expression of glycolytic enzymes (glucose transporter 1, hexokinase 2, lactate dehydrogenase A, and pyruvate kinase muscle isozyme M2). Knockdown of FSTL3 increased oxygen consumption while decreasing extracellular acidification, glucose uptake, and lactate production. Moreover, FSTL3 downregulation markedly inhibited the proliferation, migration, and invasion of CoCl Conclusions: Collectively, our findings demonstrate that ZNF454 suppresses CRC development by inhibiting FSTL3/HIF-1α-mediated glycolysis through transcriptional repression of FSTL3. This study is the first to reveal the molecular mechanism responsible for FSTL3 overexpression in CRC, providing a novel perspective for CRC treatment.
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