SLC16A1-AS1 enhances radiosensitivity and represses cell proliferation and invasion by regulating the miR-301b-3p/CHD5 a
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RESEARCH ARTICLE
SLC16A1-AS1 enhances radiosensitivity and represses cell proliferation and invasion by regulating the miR-301b-3p/CHD5 axis in hepatocellular carcinoma Shenglin Pei 1 & Zuyi Chen 2 & Huajun Tan 2 & Liwei Fan 2 & Baina Zhang 2 & Chang Zhao 2 Received: 30 March 2020 / Accepted: 2 July 2020 # Springer-Verlag GmbH Germany, part of Springer Nature 2020
Abstract Hepatocellular carcinoma (HCC), a common type of human malignancies, leads to increasing incidence and fairly high mortality. An increasing number of studies have verified that long noncoding RNAs (lncRNAs) played key roles in the development of multiple human cancers. As a biomarker, SLC16A1-AS1 has been reported in non-small cell lung cancer (NSCLC) and oral squamous cell carcinoma (OSCC). Thus, we decided to investigate whether SLC16A1-AS1 exerts its biological function in HCC. In this study, we discovered that SLC16A1-AS1 was obviously downregulated in HCC tissues and cells. Overexpression of SLC16A1-AS1 inhibited HCC cell proliferation, invasion, and epithelial-mesenchymal transition (EMT) process as well as promoted cell apoptosis. Moreover, SLC16A1-AS1 was confirmed to enhance the radiosensitivity of HCC cells. Molecular mechanism exploration suggested that SLC16A1-AS1 served as a sponge for miR-301b-3p and CHD5 was the downstream target gene of miR-301b-3p in HCC cells. Rescue assays implied that CHD5 knockdown could recover the effects of SLC16A1AS1 overexpression on HCC cellular processes. In brief, our study clarified that SLC16A1-AS1 acted as a tumor suppressor in HCC by targeting the miR-301b-3p/CHD5 axis, which may be a promising diagnostic biomarker and provide promising treatment for HCC patients. Keywords Hepatocellular carcinoma . SLC16A1-AS1 . miR-301b-3p . CHD5 . Raidosensitivity
Introduction Hepatocellular carcinoma (HCC), one of the most common malignant tumors, is a leading cause of cancer deaths worldwide (Bray et al. 2018; Ryu et al. 2014). Although numerous therapeutic strategies have been achieved, the outcome of HCC patients remains unsatisfactory due to the high frequency of metastasis and recurrence (Frenette et al. 2019; Liao Responsible Editor: Mohamed M. Abdel-Daim Electronic supplementary material The online version of this article (https://doi.org/10.1007/s11356-020-09998-1) contains supplementary material, which is available to authorized users. * Chang Zhao [email protected] 1
Department of Anesthesiology, Affiliated Tumor Hospital of Guangxi Medical University, Nanning, China
2
Department of Intervention, Affiliated Tumor Hospital of Guangxi Medical University, No. 71 Hedi Road, Qingxiu District, Nanning 530021, Guangxi, China
et al. 2018). In order to improve therapeutic options for HCC patients, it is greatly urgent to explore the potential molecular mechanism of HCC. The underlying mechanisms of long noncoding RNAs (lncRNAs) have raised much attention. LncRNAs are identified as a class of noncoding RNAs (ncRNAs) with over 200 nucleotides in length and lacking the capacity of encoding proteins (Lorenz
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