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Authors Peng J, Chen W, Chen J, Yuan Y, Zhang J, He Y
Received 13 December 2017
Accepted for publication 14 March 2018
Published 14 May 2018 Volume 2018:10 Pages 1163—1175
DOI https://doi.org/10.2147/CMAR.S159790
Checked for plagiarism Yes
Review by Single-blind
Peer reviewers approved by Dr Andrew Yee
Peer reviewer comments 2
Editor who approved publication: Dr Leylah Drusbosky
Background: Chloride
channel-3 (CLC-3) has been reported to promote the proliferation and invasion
in various tumors, yet little is known about its role in gastric cancer. In the
present study, we investigated the clinical significance of CLC-3 and its
biological role in gastric cancer.
Methods: Bioinformatic analysis, immunohistochemical staining, quantitative
real-time polymerase chain reaction and Western blot assay were used to assess
the expression of CLC-3 and its clinical significance in gastric cancer. The
biological role of CLC-3 and its underlying mechanism were detected through in
vitro experiments.
Results: CLC-3 was highly expressed in gastric cancer tissues and cell
lines, and high levels of CLC-3 were significantly associated with adverse
clinicopathological parameters and shorter overall survival time in patients
with gastric cancer. Functional studies revealed that silencing of CLC-3
decreased, while overexpression promoted, the proliferation, migration and
invasion of gastric cancer cells in vitro. Mechanistic studies suggested that
canonical TGF-β/Smad signaling pathway is involved in CLC-3-induced gastric
cancer cells proliferation, migration and invasion.
Conclusion: These findings indicate the vital role of CLC-3 in gastric cancer
progression and its potential role of a therapeutic target for treatment.
Keywords: CLC-3, gastric cancer, proliferation, migration, prognosis, TGF-β