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The Elevated ASK1 Expression Inhibits Proliferation and Invasion in Gastric Cancer HGC‐27 Cells
Author(s) -
Wan Xiaochen,
Shi Liying,
Ma Xiaohong,
Tang Haimin,
Wu Guoyou
Publication year - 2018
Publication title -
the anatomical record
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.23906
Subject(s) - ask1 , cell migration , cell growth , cancer research , apoptosis , cancer cell , signal transduction , cell , microbiology and biotechnology , biology , cancer , chemistry , biochemistry , mitogen activated protein kinase kinase , genetics , protein kinase c
This study aimed to evaluate the effects and mechanism of action of ASK1 gene on the growth and migration of gastric cancer (GC) cells. Total RNA was extracted from the gastric cell lines and GC tissues. The expression level of ASK1, and the association between ASK1 expression and clinicopathological characteristics was assessed by real‐time polymerase chain reaction. The effects of ASK1 on the proliferation of HGC–27 cells were assessed by the CCK–8 assay. In addition, the effects of ASK1 on the migration of HGC–27 cells were analyzed by the migration assay using transwell chambers. The expression levels of signaling proteins related to cell migration were detected by Western blotting. Although no significant differences were observed in the expression levels of ASK1 between the GC tissue samples and the normal tissue samples ( P = 0.241), ASK1 expression correlated with tumor lymph node metastasis ( P = 0.008). Furthermore, ASK1 inhibited proliferation and migration of HGC–27 cells. The increase in the expression of ASK1 in HGC–27 cells induced the activation of the JNK and p38 signaling pathways. The findings demonstrated that increased ASK1 expression level inhibited migration and proliferation of HGC–27 gastric cancer cells, whereas the possible mechanism of action may be attributed to the activation of the JNK and p38 signaling pathways. Anat Rec, 301:1815–1819, 2018. © 2018 Wiley Periodicals, Inc.