BASIC RESEARCH
Functions of the AP-2α gene in activating apoptosis and inhibiting proliferation of gastric cancer cells both in vitro and in vivo
Submission date: 2015-03-16
Final revision date: 2015-07-01
Acceptance date: 2015-07-20
Online publication date: 2017-10-31
Publication date: 2017-10-30
Arch Med Sci 2017;13(6):1255–1261
KEYWORDS
TOPICS
ABSTRACT
Introduction: This study was designed to investigate the potential function of the activating protein 2α (AP-2α) gene in controlling the proliferation and apoptosis of gastric cancer.
Material and methods: Gastric cancer cell line MCG-803 cells and normal cell line GES-1 cells were selected to transfect pcDNA3.1(+)-AP-2α and pcDNA3.1(+) plasmids, respectively. Both mRNA and protein levels of AP-2α in each group transfected with the pcDNA3.1(+)-AP-2α plasmids were up-regulated after 48 h by real-time PCR and Western blotting analysis, leading to marked proliferation inhibition and significant cell cycle arrest.
Results: pcDNA3.1(+)-AP-2α reduced tumor tissue growth in a subcutaneous tumor gastric carcinoma nude mouse model. Protein over-expression of AP-2α in the nude mouse model was accompanied by down-regulation of Blc-2 and ErbB2, resulting in the up-regulation of caspase-3, -8, and -9, ERα and p21WAF1/CIP1.
Conclusions: The reintroduction of the AP-2α gene by pcDNA3.1 could inhibit gastric tumor growth in vitro and in vivo, which may be an alternative future therapeutic molecular target for human gastric cancer.
Material and methods: Gastric cancer cell line MCG-803 cells and normal cell line GES-1 cells were selected to transfect pcDNA3.1(+)-AP-2α and pcDNA3.1(+) plasmids, respectively. Both mRNA and protein levels of AP-2α in each group transfected with the pcDNA3.1(+)-AP-2α plasmids were up-regulated after 48 h by real-time PCR and Western blotting analysis, leading to marked proliferation inhibition and significant cell cycle arrest.
Results: pcDNA3.1(+)-AP-2α reduced tumor tissue growth in a subcutaneous tumor gastric carcinoma nude mouse model. Protein over-expression of AP-2α in the nude mouse model was accompanied by down-regulation of Blc-2 and ErbB2, resulting in the up-regulation of caspase-3, -8, and -9, ERα and p21WAF1/CIP1.
Conclusions: The reintroduction of the AP-2α gene by pcDNA3.1 could inhibit gastric tumor growth in vitro and in vivo, which may be an alternative future therapeutic molecular target for human gastric cancer.
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