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Authors Dang SC, Wang F, Qian XB, Abdul M, Naseer QA, Jin W, Hu R, Gu Q, Gu M
Received 2 October 2018
Accepted for publication 19 December 2018
Published 24 January 2019 Volume 2019:12 Pages 795—803
DOI https://doi.org/10.2147/OTT.S189521
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Justinn Cochran
Peer reviewer comments 2
Editor who approved publication: Dr William Cho
Purpose: The
expression of microRNA-505 (miR-505) has been investigated in various cancers;
however, its effect and mechanism in relation to gastric cancer (GC) are yet to
be determined. Thus, the current evaluation aimed to examine the expression and
potential role of miR-505 in GC.
Materials and methods: Quantitative
real-time PCR was carried out to analyze miR-505 expression in GC cells and
tissues. We observed that miR-505 is differentially expressed in GC cells
following transfection of its mimics or inhibitors. Changes in cell invasion,
cell proliferation, and epithelial–mesenchymal transition markers were
measured.
Results: These
findings indicated that miR-505 expression is downregulated in both GC cell
lines and GC tissues. In addition, knockdown miR-505 induced the invasion and
proliferation of GC cells. Transfection of miR-505 mimics led to an elevation
in N-cadherin expression but a decrease in E-cadherin expression. Furthermore,
we have shown that miR-505 binds to the 3'-UTR region of Polo-like kinase-1.
Conclusion: Our
results indicated that miR-505 suppresses GC cell proliferation and invasion;
it may be a valuable candidate gene for seeking therapy strategy for GC.
Keywords: MicroRNA-505,
EMT, polo-like kinase-1, gastric cancer
