ArticleMolecular medicine (Cambridge, Mass.)2024
BTF3 affects hepatocellular carcinoma progression by transcriptionally upregulating PDCD2L and inactivating p53 signaling.
Article in Molecular medicine (Cambridge, Mass.), 2024. 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.
- PDCD2L overexpression represents an unfavorable prognostic marker and its inhibition shows promising therapeutic potential for gastric cancer.Cancer biomarkers : section A of Disease markers · 2025Article
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4 authors.
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Abstract
Hepatocellular carcinoma (HCC) is one of the most common malignant tumors, with the characteristics of high mortality and low 5-year survival rate. The potential role of BTF3 and PDCD2L in HCC remains unclear. Our study found that BTF3 expression was upregulated in hepatocellular carcinoma tissues, and its high expression was associated with poor prognosis. Knockdown of BTF3 significantly inhibited proliferation and promoted apoptosis of hepatocellular carcinoma cells by cell function assay. Mechanistically, BTF3 plays an oncogenic role by regulating the transcriptional expression of PDCD2L, which promotes proliferation and inhibits apoptosis of HCC cells by restraining the p53 pathway. In conclusion, our results suggest that BTF3 induces malignant progression of HCC by acting as a transcription factor that promotes the transcription of PDCD2L and influences the p53 pathway and that the BTF3/PDCD2L/P53 axis may be a future therapeutic strategy for HCC patients.
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