Abstract
During recent years, long noncoding RNAs (lncRNAs) have received focal attention due to their important function in cancer regulation. Though the relation between lncRNA SNAI3-AS1 and the development of hepatocellular carcinoma (HCC) has been described in our previous study, the role and the exact mechanism of SNAI3-AS1 are still unclear. In this study, qRT-PCR analysis revealed that the expression of SNAI3-AS1 was elevated and was correlated with the levels of PEG10 in HCC tissues. Through functional experiments, we determined that knockdown of SNAI3-AS1 and PEG10 inhibited the proliferation and metastasis, whereas overexpression of SNAI3-AS1 and PEG10 promoted the proliferation and metastasis of HCC cells. In addition, rescue experiments confirmed that upregulation of PEG10 partially restored cell function inhibition induced by SNAI3-AS1 knockdown. Therefore, we hypothesized that PEG10 may be regulated by SNAI3-AS1, which in turn mediates the malignant biological processes of HCC cells regulated by PEG10. Further bioinformatics analysis and mechanistic experiments showed that SNAI3-AS1 functions as a competing endogenous RNA (ceRNA) to activate PEG10 by acting as a sponge for miR-27-3p and miR-34a-5p. In summary, our study revealed that SNAI3-AS1 is a tumor regulator of PEG10 in the progression of HCC, and may contribute to the improvement of HCC diagnosis and therapy.
Highlights
Hepatocellular carcinoma (HCC) is the principal cause of mortality among cirrhotic patients and the third cause of cancer-related death worldwide[1,2]
These data indicated that overexpressed SNAI3AS1 and Paternally expressed gene 10 (PEG10) were associated with the development and progression of HCC
The dysregulation of long noncoding RNAs (lncRNAs) in the tumor reflects the extent of disease progression to some extent and maybe an independent risk factor for predicting the prognosis of patients[18,19,20]
Summary
Hepatocellular carcinoma (HCC) is the principal cause of mortality among cirrhotic patients and the third cause of cancer-related death worldwide[1,2]. Liver cancer is divided into cholangiocarcinoma, HCC, and mixed HCC according to different cell origin, and among them, HCC is the most common type. The character of fast growth and unobvious symptoms in the early stage takes the main charge for the unfavorable diagnosis and prognosis of HCC. Hepatocarcinogenesis is often described as a complex step involving multiple genes and genetic alterations that lead to malignant transformation of hepatocytes[3,4,5]. Despite significant advances in diagnosis and management, the molecular biology of HCC remains poorly understood. Looking for crucial tumorrelated molecular and identifying the underlying mechanisms in HCC are urgently needed for molecular diagnostics and targeted therapies
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