已发表论文

上调 CKAP2L 表达可促进肺腺癌的侵袭,并且与预后不良有关

 

Authors Xiong GS, Li LY, Chen XB, Song SN, Zhao YP, Cai WK, Peng JP

Received 1 August 2018

Accepted for publication 19 December 2018

Published 12 February 2019 Volume 2019:12 Pages 1171—1180

DOI https://doi.org/10.2147/OTT.S182242

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Justinn Cochran

Peer reviewer comments 2

Editor who approved publication: Dr Leo Jen-Liang Su

Aim: The purpose of this study is to consider the function of cytoskeleton-associated protein 2-like (CKAP2L) in lung adenocarcinoma (LAD) development and its prognostic value.
Methods: The mRNA expression of CKAP2L and its correlation with clinical factors in LAD patients were analyzed from the data taken from The Cancer Genome Atlas and The First Affiliated Hospital of Kunming Medical University. We constructed H460 and A549 cell lines with silenced CKAP2L using RNA interference. Cell counting kit-8 assay and colony formation assays were carried out to determine the function of CKAP2L in H460 and A549 cell proliferation. Transwell and wound healing assays were applied to determine the effect of CKAP2L on H460 and A549 cell invasion and migration. The influences of CKAP2L on mitogen-activated protein kinase signaling pathway-related proteins were tested by Western blotting.
Results: CKAP2L expression is enhanced in LAD tissues and is predictive of poor prognosis in LAD patients. High expression of CKAP2L is associated with stage (<0.001), lymph node status (=0.002), and metastasis (=0.025). Depletion of CKAP2L dramatically suppressed the proliferation, migration, and invasion of H460 and A549 cells. Moreover, the ratio of p-MEK/MEK and p-ERK/ERK reduced obviously in A549 cells after depleting CKAP2L. 
Conclusion: Our findings implied that CKAP2L might be a promoter of LAD and could serve as a predictor for LAD patients.
Keywords: CKAP2L, prognosis, lung adenocarcinoma, migration, proliferation




Figure 3 Depleting CKAP2L suppresses A549 and H460 cell proliferation.