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DLX6‐AS1 accelerates cell proliferation through regulating miR ‐497‐5p/ SNCG pathway in prostate cancer
Author(s) -
Zhu Xu,
Ma Xingxin,
Zhao Shuli,
Cao Zhigang
Publication year - 2021
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.23036
Subject(s) - gene knockdown , oncogene , cancer research , downregulation and upregulation , cell growth , prostate cancer , apoptosis , cell , microbiology and biotechnology , chemistry , cancer , biology , cell cycle , gene , biochemistry , genetics
Prostate cancer (PCa) has become the second leading cause of cancer‐related mortality in males worldwide. Although the long noncoding RNA DLX6‐AS1 has been recognized to be an oncogene in multiple cancers, the biological function and regulatory mechanism of DLX6‐AS1 in prostate cancer are still obscure. In the present study, we observed that DLX6‐AS1 was significantly upregulated in PCa tissues and cells. Knockdown of DLX6‐AS1 inhibited PCa progression by suppressing cell proliferation and accelerating cell apoptosis. Molecular mechanism exploration indicated that DLX6‐AS1 acted as a sponge for miR‐497‐5p and synuclein gamma (SNCG) was a downstream target gene of miR‐497‐5p. In addition, there was a negative correlation between DLX6‐AS1 and miR‐497‐5p in PCa tissues. Rescue assays showed that SNCG overexpression could partially recover DLX6‐AS1 knockdown‐mediated inhibition of progression in PCa. Furthermore, xenograft tumor model was established to determine the role of DLX6‐AS1 in PCa tumor growth and the results suggested that DLX6‐AS1 could facilitate tumor growth by regulating SNCG in vivo. In conclusion, our study investigated the biological function and underlying mechanism of DLX6‐AS1 in PCa and validated that DLX6‐AS1 functioned as an oncogene through miR‐497‐5p/SNCG axis.