TY - JOUR
T1 - DAB2IP downregulation enhances the proliferation and metastasis of human gastric cancer cells by derepressing the ERK1/2 pathway
AU - Sun, Liang
AU - Yao, Yizhou
AU - Lu, Ting
AU - Shang, Zengfu
AU - Zhan, Shenghua
AU - Shi, Weiqiang
AU - Pan, Guofeng
AU - Zhu, Xinguo
AU - He, Songbing
N1 - Funding Information:
This present study was supported by Project of Nature Science Foundation of China (81672348), Natural Science Foundation of Jiangsu Province of China (BK2016255), Six Major Talent Peak Project of Jiangsu Province of China (2015-WSW-014), Six One Project for Advanced Medical Talent of Jiangsu Province of China (LGY2016031), and Jiangsu Provincial Medical Youth Talent (QNRC2016735).
Publisher Copyright:
Copyright © 2018 Liang Sun et al.
PY - 2018
Y1 - 2018
N2 - DAB2IP (DOC2/DAB2 interactive protein) is downregulated in several cancer types, and its downregulation is involved in tumor cell proliferation, apoptosis, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to investigate the potential role of DAB2IP in the development and progression of gastric cancer. DAB2IP levels were analyzed in human gastric cancer and adjacent normal tissues by Western blots and immunohistochemistry. Potential roles of DAB2IP in regulating gastric cancer cell growth and metastasis were examined by genetic manipulation in vitro. The molecular signaling was determined to understand the mechanisms of observed DAB2IP effects. DAB2IP level is lower in gastric cancer tissues as compared to paired normal tissues. Knockdown of DAB2IP enhanced gastric cancer cell growth and metastasis in vitro and promoted EMT progress at both protein and mRNA levels. Silencing DAB2IP activated extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, and the enhanced proliferation and migration ability induced by DAB2IP knockdown were reduced after incubation with U0126 in SGC7901 gastric cancer cells. Inhibition of DAB2IP enhances gastric cancer cell growth and metastasis through targeting the ERK1/2 signaling, indicating that it may serve as a potential target for treatment of gastric cancer.
AB - DAB2IP (DOC2/DAB2 interactive protein) is downregulated in several cancer types, and its downregulation is involved in tumor cell proliferation, apoptosis, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to investigate the potential role of DAB2IP in the development and progression of gastric cancer. DAB2IP levels were analyzed in human gastric cancer and adjacent normal tissues by Western blots and immunohistochemistry. Potential roles of DAB2IP in regulating gastric cancer cell growth and metastasis were examined by genetic manipulation in vitro. The molecular signaling was determined to understand the mechanisms of observed DAB2IP effects. DAB2IP level is lower in gastric cancer tissues as compared to paired normal tissues. Knockdown of DAB2IP enhanced gastric cancer cell growth and metastasis in vitro and promoted EMT progress at both protein and mRNA levels. Silencing DAB2IP activated extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, and the enhanced proliferation and migration ability induced by DAB2IP knockdown were reduced after incubation with U0126 in SGC7901 gastric cancer cells. Inhibition of DAB2IP enhances gastric cancer cell growth and metastasis through targeting the ERK1/2 signaling, indicating that it may serve as a potential target for treatment of gastric cancer.
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U2 - 10.1155/2018/2968252
DO - 10.1155/2018/2968252
M3 - Article
C2 - 29743885
AN - SCOPUS:85056214791
SN - 1687-6121
VL - 2018
JO - Gastroenterology Research and Practice
JF - Gastroenterology Research and Practice
M1 - 2968252
ER -