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LncRNA SNHG16 drives proliferation, migration, and invasion of lung cancer cell through modulation of miR-520/VEGF axis.

AbstractOBJECTIVE:
Long non-coding RNAs (lncRNAs) have been shown to have important effects on various biological behavior of human diseases. Although increasing lncRNAs have been explored in human cancers, there are still countless lncRNA to be mined. The purpose of this study was to investigate the effect of lncRNA SNHG16 on the proliferation and metastasis of lung cancer cells.
PATIENTS AND METHODS:
RT-qPCR was used to analyze the expression patterns of SNHG16, miR-520 and VEGF. MTT and transwell methods were used to detect the effect of SNHG16 on cell migration. The association between SNHG16, miR-520 and VEGF was analyzed by bioinformatics analysis and Dual-Luciferase verification reporter analysis. Finally, lung cancer cells have demonstrated the role of SNHG16-miR-520-VEGF in the cell biological behavior axis.
RESULTS:
Compared with normal cells, SNHG16 is highly expressed in lung cancer cells. Silent SNHG16 has a negative effect on the migration of lung cancer cells.
CONCLUSIONS:
LncRNA SNHG16 as ceRNA up-regulates VEGF in lung cancer cells by binding to miR-520. LncRNA SNHG16 as ceRNA promotes the migration of lung cancer cells by regulating the miR-520/VEGF axis.
AuthorsL Chen, C-H Qiu, Y Chen, Y Wang, J-J Zhao, M Zhang
JournalEuropean review for medical and pharmacological sciences (Eur Rev Med Pharmacol Sci) Vol. 24 Issue 18 Pg. 9522-9531 (09 2020) ISSN: 2284-0729 [Electronic] Italy
PMID33015794 (Publication Type: Journal Article)
Chemical References
  • MIRN520 microRNA, human
  • MicroRNAs
  • RNA, Long Noncoding
  • SNHG16 lncRNA, human
  • VEGFA protein, human
  • Vascular Endothelial Growth Factor A
Topics
  • Cell Movement
  • Cell Proliferation
  • Female
  • Humans
  • Lung Neoplasms (metabolism, pathology)
  • Male
  • MicroRNAs (genetics, metabolism)
  • Middle Aged
  • RNA, Long Noncoding (genetics, metabolism)
  • Tumor Cells, Cultured
  • Vascular Endothelial Growth Factor A (genetics, metabolism)

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