ArticleCancer medicine2023
Sulfotransferase 1C2 promotes hepatocellular carcinoma progression by enhancing glycolysis and fatty acid metabolism.
Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- SULT1E1 suppresses hepatocellular carcinoma progression via activation of the TGF-β/SMAD signaling pathway and cell cycle arrest.BMC gastroenterology · 2026Article
- An integrated investigation of sulfotransferases (SULTs) in hepatocellular carcinoma and identification of the role of SULT2A1 on stemness.Apoptosis : an international journal on programmed cell death · 2024Article
- Article
- Sulfotransferase 1C2 promotes hepatocellular carcinoma progression by enhancing glycolysis and fatty acid metabolism.Cancer medicine · 2023Article
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Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHepatocellular carcinoma (HCC) is aggressive liver cancer. Despite advanced imaging and other diagnostic measures, HCC in a significant portion of patients had reached the advanced stage at the first diagnosis. Unfortunately, there is no cure for advanced HCC. As a result, HCC is still a leading cause of cancer death, and there is a pressing need for new diagnostic markers and therapeutic targets.
methodsWe investigated sulfotransferase 1C2 (SUTL1C2), which we recently showed was overexpressed in human HCC cancerous tissues. Specifically, we analyzed the effects of SULT1C2 knockdown on the growth, survival, migration, and invasiveness of two HCC cell lines, i.e., HepG2 and Huh7 cells. We also studied the transcriptomes and metabolomes in the two HCC cell lines before and after SULT1C2 knockdown. Based on the transcriptome and metabolome data, we further investigated the SULT1C2 knockdown-mediated shared changes, i.e., glycolysis and fatty acid metabolism, in the two HCC cell lines. Finally, we performed rescue experiments to determine whether the inhibitory effects of SULT1C2 knockdown could be rescued via overexpression.
resultsWe showed that SULT1C2 overexpression promoted the growth, survival, migration, and invasiveness of HCC cells. In addition, SULT1C2 knockdown resulted in a wide range of gene expression and metabolome changes in HCC cells. Moreover, analysis of shared alterations showed that SULT1C2 knockdown significantly suppressed glycolysis and fatty acid metabolism, which could be rescued via SULT1C2 overexpression.
conclusionsOur data suggest that SULT1C2 is a potential diagnostic marker and therapeutic target for human HCC.
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