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DLX6-AS1 accelerates cell proliferation through regulating miR-497-5p/SNCG pathway in prostate cancer.

Abstract
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.
AuthorsXu Zhu, Xingxin Ma, Shuli Zhao, Zhigang Cao
JournalEnvironmental toxicology (Environ Toxicol) Vol. 36 Issue 3 Pg. 308-319 (Mar 2021) ISSN: 1522-7278 [Electronic] United States
PMID33035382 (Publication Type: Journal Article)
Copyright© 2020 Wiley Periodicals LLC.
Chemical References
  • DLX6 protein, human
  • Homeodomain Proteins
  • MIRN497 microRNA, human
  • MicroRNAs
  • Neoplasm Proteins
  • RNA, Long Noncoding
  • SNCG protein, human
  • gamma-Synuclein
Topics
  • Apoptosis
  • Cell Proliferation (genetics)
  • Disease Progression
  • Gene Expression Regulation, Neoplastic
  • Homeodomain Proteins (genetics, metabolism)
  • Humans
  • Male
  • MicroRNAs (metabolism)
  • Neoplasm Proteins (genetics)
  • Prostatic Neoplasms (genetics)
  • RNA, Long Noncoding (genetics)
  • Up-Regulation
  • gamma-Synuclein (genetics, metabolism)

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