Article Publish Status: FREE
Abstract Title:

Suppression of lncRNA MALAT1 by betulinic acid inhibits hepatocellular carcinoma progression by targeting IAPs via miR-22-3p.

Abstract Source:

Clin Transl Med. 2020 Oct ;10(6):e190. PMID: 33135336

Abstract Author(s):

Feiyu Chen, Zhangfeng Zhong, Hor Yue Tan, Wei Guo, Cheng Zhang, Chien-Shan Cheng, Ning Wang, Junguo Ren, Yibin Feng

Article Affiliation:

Feiyu Chen


Betulinic acid (BA) is a natural product extracted from a broad range of medicinal and edible herbal plants. Previous studies showed that BA induces cell death in tumors derived from multiple tissues; however, the underlying mechanism remains obscure. The present study aimed to study the effects of BA on autophagy and apoptosis of hepatocellular carcinoma (HCC). Human HCC cell lines and orthotopic HCC implanted mice were employed to examine the BA-induced tumor suppression; RTlong noncoding RNA (lncRNA) PCR array and database analysis were used to explore the possible mechanisms; validation of pathways was performed using siRNA and miRNA inhibitors. The results indicated that BA regulated autophagy and induced apoptosis in HCC. The degradation of inhibitor of apoptosis proteins (IAPs), the conversion of LC3-I to LC3-II, and p62 accumulation were enhanced by BA, thereby suggesting that the downregulation of IAPs and autophagic cell death are induced by BA. The addition of autophagy and lysosomal inhibitors indicated that BA induced autophagy-independent apoptosis via degradation of IAPs. Moreover, RTlncRNA PCR array and database analysis suggested that BA downregulated the levels of lncRNA MALAT1, which is considered to be an oncogene. Further investigations demonstrated that lncRNA MALAT1 functioned as a ceRNA (competing endogenous RNA) to contribute to BA-mediated degradation of IAPs by sponging miR-22-3p. Therefore, BA could be developed as a potential anticancer agent for HCC.

Study Type : In Vitro Study

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