已发表论文

C14orf159 通过灭活 ERK 信号传导抑制胃癌细胞的侵袭和增殖

 

Authors Zhu YM, Li Q, Gao XZ, Meng X, Sun LL, Shi Y, Lu ET, Zhang Y

Received 10 June 2018

Accepted for publication 17 January 2019

Published 19 February 2019 Volume 2019:11 Pages 1717—1723

DOI https://doi.org/10.2147/CMAR.S176771

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Justinn Cochran

Peer reviewer comments 2

Editor who approved publication: Dr Kenan Onel

Background: C14orf159, a new protein, has been identified recently. But its expression in tissues and clinicopathologic correlation is still unknown. 
Patients and methods: We carried out immunohistochemistry staining in 144 gastric cancer cases in this study. Then Western blot was used to detect the expression of protein. MTT and matrigel invasion assay were used to assess the biological effects.
Results: The immunohistochemical results indicated that the expression of C14orf159 in normal gastric mucosa close to cancer tissue was remarkably higher than that in stomach carcinoma samples (63.9% and 34.7%, respectively, <0.001). Negative C14orf159 expression was dramatically related to high TNM stages (=0.033) and positive lymph node metastasis (=0.008). Once C14orf159 was overexpressed, the expression levels of phosphorylated ERK and its regulated downstream molecules, such as Snail, phosphorylated P90RSK and Cyclin D1, were decreased, while the expression level of E-cadherin was increased. Finally, the invasion and proliferation capacity of gastric cancer cells was inhibited. 
Conclusion: In other words, loss of C14orf159 is associated with the progression of gastric cancer. The role of C14orf159 in repression of proliferation and invasion may be due to resuming E-cadherin and abolishing Snail and Cyclin D1 expression through inactivating ERK–P90RSK pathway.
Keywords: C14orf159, gastric cancer, ERK, invasion, proliferation




Figure 1 The expression of C14orf159 in both gastric cancer specimens and cell lines.