ArticleThe Kaohsiung journal of medical sciences2026
Role of ZNF652 in Regulating Hepatocellular Carcinoma Cell Proliferation and Apoptosis via the circRHOT1/SLC38A6 Axis.
Article in The Kaohsiung journal of medical sciences, 2026. 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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Who cites it
1 citing paper in PubMed.
- Role of ZNF652 in Regulating Hepatocellular Carcinoma Cell Proliferation and Apoptosis via the circRHOT1/SLC38A6 Axis.The Kaohsiung journal of medical sciences · 2026Article
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8 authors.
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Abstract
Hepatocellular carcinoma (HCC) is a heterogeneous malignancy characterized by high mortality rates. This article presents a discussion of the role of ZNF652 in HCC cell proliferation and apoptosis, thereby identifying a new target for HCC treatment. The expression levels of ZNF652, circRHOT1, and SLC38A6 in HCC and healthy cells were analyzed. Cell proliferation and apoptosis were subsequently validated. The binding relationships between ZNF652 and the circRHOT1 promoter and between circRHOT1 and KAT5 were validated. The recruitment of KAT5 and H3K27ac to the SLC38A6 promoter was assessed via ChIP. Combined experiments were carried out to verify the role of the circRHOT1/SLC38A6 pathway in HCC cell proliferation and apoptosis. ZNF652, circRHOT1, and SLC38A6 were upregulated in HCC cells. ZNF652 silencing inhibited HCC cell proliferation but promoted apoptosis. Mechanistically, ZNF652 increased circRHOT1 expression at the transcriptional level and recruited KAT5 to the SLC38A6 promoter to increase H3K27ac enrichment and activate SLC38A6 expression. Combined experiments revealed that overexpression of circRHOT1 or SLC38A6 could alleviate the effects of ZNF652 silencing on HCC cell proliferation and apoptosis. In conclusion, ZNF652 transcriptionally activated circRHOT1 expression, recruited KAT5 to the SLC38A6 promoter, increased H3K27ac enrichment, and activated SLC38A6 expression, thus promoting HCC cell proliferation and inhibiting apoptosis.
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