Abstract & Article Details
Research Article • Vol.4, Issue 4 • ISSN: 2766-2276 • Open Access • CC BY 4.0
Overexpression miR-642 Inhibits Cell Migration and Proliferation by Regulation of KRT19 and Clinical Prognosis Value in Gastric Cancer
Abstract
Objective: To investigate the expression of miR-642 in gastric cancer and its mechanism in the proliferation and migration.
Methods: qRT-PCR was used to detect the expression of miR-642 in gastric cancer. Dual luciferase gene reporting system was used to verify the direct regulatory effect of miR-642 on KRT19 3' UTR. The mRNA and protein levels of KRT19 gene after transfection were detected by qRT-PCR and Western blot. The proliferation of miR-642 was detected by IncucyteS long term dynamic cell observation. Kaplan-Meier method was used to analyze the relationship between miR-642 expression level and prognosis in patients with gastric cancer.
Results: The expression of miR-642 in gastric cancer tissues was lower than that in paracancer tissues. The fluorescence intensity of MGC803 cells was significantly decreased after co-transfection of miR-642 mimics and wild-type KRT19-3 'UTR recombinant vector. The expression levels of KRT19 mRNA and protein were significantly decreased after transfected with miR-642 mimics and KRT19 siRNA. Western blot analysis of PTEN, Akt and mTOR proteins showed different expression. Prognostic survival analysis showed that gastric cancer patients with low expression of miR-642 had shorter survival.
Conclusion: miR-642 expression can negatively regulate the target gene KRT19.
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How to Cite
Article Information
| Journal | Journal of Biomedical Research & Environmental Sciences (JBRES) |
|---|---|
| ISSN | 2766-2276 |
| DOI | DOI 10.37871/jbres1713 |
| Volume / Issue | Vol. 4, Issue 4 |
| Published | April 3, 2023 |
| Article Type | Research Article |
| Pages | 579-589 |
| License | CC BY 4.0 — Open Access |
| Publisher | SciRes Literature LLC, Sheridan, WY, USA |
| Language | English |
Published under CC BY 4.0 — free to share, copy, adapt, and redistribute with attribution.