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Authors Zhao Y, Dong Q, Wang E
Received 27 September 2016
Accepted for publication 17 December 2016
Published 20 February 2017 Volume 2017:10 Pages 1049—1058
DOI https://doi.org/10.2147/OTT.S123324
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Amy Norman
Peer reviewer comments 2
Editor who approved publication: Dr Ingrid Espinoza
Abstract: MicroRNA-320 (miR-320) downregulation has been reported in several human
cancers. Until now, its expression pattern and biological roles in human cancer
remain unknown. This study aims to clarify its clinical expression pattern and
biological function in gastric cancers. We found miR-320 level was
downregulated in gastric cancer tissues. miR-320 mimic was transfected in SGC-7901
cells with low endogenous expression. miR-320 inhibitor was used in BGC-823
cells with high endogenous expression. We found that miR-320 inhibited SGC-7901
proliferation and invasion, with decreased expression of cyclin D1 and MMP9 at
both mRNA and protein levels. We also found that miR-320 mimic downregulated
chemoresistance and cell survival of gastric cancer cells when treated with
5-fluorouracil. miR-320 inhibitor displayed the opposite effects in BGC-823
cell line. In addition, we discovered that miR-320 mimic could inhibit AKT and
ERK activity. By using luciferase reporter assay, we found that CRKL serves as
the target of miR-320. miR-320 mimic downregulated CRKL expression, whereas
miR-320 inhibitor upregulated CRKL expression. miR-320 suppressed
CRKL-3'-untranslated region reporter intensity in SGC-7901 cells. Furthermore,
CRKL depletion abrogated the effects of miR-320. In gastric cancer tissues, we
observed a negative correlation between CRKL and miR-320. In conclusion, our
study demonstrated that downregulation of miR-320 was closely related with
malignant progression of gastric cancer. miR-320 inhibits proliferation,
invasion, and chemoresistance through ERK and AKT signaling by targeting CRKL.
Keywords: gastric cancer, miR-320, CRKL, proliferation,
invasion