The roles of BTG3 expression in gastric cancer: a potential marker for carcinogenesis and a target molecule for gene therapy
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Wen-feng Gou1, Xue-feng Yang1, Dao-fu Shen1, Shuang Zhao1, Yun-peng Liu2, Hong-zhi Sun1, Yasuo Takano3, Rong-jian Su4, Jun-sheng Luo1 and Hua-chuan Zheng1
1 Cancer Research Center, Key Laboratory of Brain and Spinal Cord Injury of Liaoning Province, and Laboratory Animal Center, The First Affiliated Hospital of Liaoning Medical University, Jinzhou, China
2 Department of Oncological Medicine, The First Affiliated Hospital of China Medical University, Shenyang, China
3 School of Health Science, Tokyo University of Technology, Ohta-ku, Tokyo
4 Experimental Center, Liaoning Medical University, Jinzhou, China
Hua-chuan Zheng, email:
Keywords: gastric cancer, BTG3, carcinogenesis, pathobiological behaviors, gene therapy
Received: February 11, 2015 Accepted: March 10, 2015 Published: March 30, 2015
BTG (B-cell translocation gene) can inhibit cell proliferation, metastasis and angiogenesis, cell cycle progression, and induce differentiation in various cells. Here, we found that BTG3 overexpression inhibited proliferation, induced S/G2 arrest, differentiation, autophagy, apoptosis, suppressed migration and invasion in MKN28 and MGC803 cells (p < 0.05). BTG3 transfectants showed a higher mRNA expression of p27, Bax, 14-3-3, Caspase-3, Caspase-9, Beclin 1, NF-κB, IL-1, -2, -4, -10 and -17, but a lower mRNA expression of p21, MMP-9 and VEGF than the control and mock (p < 0.05). At protein level, BTG3 overexpression increased the expression of CDK4, AIF, LC-3B, Beclin 1 and p38 (p < 0.05), but decreased the expression of p21 and β-catenin in both transfectants (p < 0.05). After treated with cisplatin, MG132, paclitaxel and SAHA, both BTG3 transfectants showed lower viability and higher apoptosis than the control in both time- and dose-dependent manners (p < 0.05). BTG3 expression was restored after 5-aza-2’-deoxycytidine or MG132 treatment in gastric cancer cells. BTG3 expression was decreased in gastric cancer in comparison to the adjacent mucosa (p < 0.05), and positively correlated with venous invasion and dedifferentiation of cancer (p < 0.05). It was suggested that BTG3 expression might contribute to gastric carcinogenesis. BTG3 overexpression might reverse the aggressive phenotypes and be employed as a potential target for gene therapy of gastric cancer.
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