Hepatocellular carcinoma (HCC) presents a great burden for patients worldwide, and metastasis of HCC remains problematic. Arsenic trioxide is a traditional drug that has shown excellent efficacy when applied as cancer therapy. Our study explored the antimetastatic mechanism of arsenic trioxide in HCC. We investigated changes in pyruvate kinase muscle isoform 2 (PKM2) and maternal expression gene 3 (MEG3) following treatment with arsenic trioxide in HCC cells. Consequently, arsenic trioxide negatively regulated PKM2 and positively regulated MEG3. We explored migration ability and the expression of the epithelial to mesenchymal transition (EMT)-related biomarkers E-cadherin, N-cadherin and Vimentin by silencing MEG3 under arsenic trioxide treatment. The wound healing assay showed that arsenic trioxide inhibited the migration of HCC, but silencing MEG3 partially reversed this effect. On the other hand, the EMT-related biomarkers are alleviated under the treatment of arsenic trioxide, but this effect deteriorated when MEG3 is silenced. In conclusion, our study demonstrates a novel mechanism by which arsenic trioxide inhibits EMT in hepatocellular carcinoma by promoting lncRNA MEG3 and PKM2 negatively regulating MEG3.
Keywords: Arsenic trioxide; Epithelial to mesenchymal transition; Hepatocellular carcinoma; Maternally expressed gene 3; Pyruvate kinase muscle isoform 2.
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