Role and mechanism of miR-222 in arsenic-transformed cells for inducing tumor growth
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Min Wang1, Xin Ge1,*, Jitai Zheng1,*, Dongmei Li1,4, Xue Liu1, Lin Wang1,4, Chengfei Jiang1, Zhumei Shi1, Lianju Qin3, Jiayin Liu3, Hushan Yang5, Ling-Zhi Liu6, Jun He6, Linlin Zhen2, Bing-Hua Jiang1,6
1State Key Laboratory of Reproductive Medicine, Department of Pathology, and Collaborative Innovation Center for Cancer Personalized Medicine, Cancer Center, Nanjing Medical University, Nanjing, Jiangsu, China
2Department of Breast and Thyroid Surgery, Huai'an First People's Hospital, Huai'an, Jiangsu, China
3Center of Clinical Reproductive Medicine, Jiangsu Province Hospital, Nanjing, Jiangsu, China
4Ninggao Personalized Medicine and Technology Innovation Center, Nanjing, Jiangsu, China
5Division of Population Science, Department of Medical Oncology, Thomas Jefferson University, Philadelphia, PA, USA
6Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA, USA
*These authors contributed equally to this work
Linlin Zhen, e-mail: firstname.lastname@example.org
Keywords: BEAS-2B cells, miR-222, PTEN, ARID1A, tumor growth
Received: September 26, 2015 Accepted: January 14, 2016 Published: February 20, 2016
High levels of arsenic in drinking water, soil, and air are associated with the higher incidences of several kinds of cancers worldwide, but the mechanism is yet to be fully discovered. Recently, a number of evidences show that dysregulation of microRNAs (miRNAs) induces carcinogenesis. In this study, we found miR-222 was upregulated in arsenic-transformed human lung epithelial BEAS-2B cells (As-T cells). Anti-miR-222 inhibitor treatment decreased cell proliferation, migration, tube formation, and induced apoptosis. In addition, anti-miR-222 inhibitor expression decreased tumor growth in vivo. We also found that inhibition of miR-222 induced the expression of its direct targets ARID1A and phosphatase and tensin homolog deleted on chromosome 10 (PTEN), and activated apoptosis of As-T cells in part through ARID1A downregulation. These results indicate that miR-222 plays an important role in arsenic-induced tumor growth.
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