Oncotarget

Research Papers:

Role and mechanism of miR-222 in arsenic-transformed cells for inducing tumor growth

Min Wang, Xin Ge, Jitai Zheng, Dongmei Li, Xue Liu, Lin Wang, Chengfei Jiang, Zhumei Shi, Lianju Qin, Jiayin Liu, Hushan Yang, Ling-Zhi Liu, Jun He, Linlin Zhen and Bing-Hua Jiang _

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Oncotarget. 2016; 7:17805-17814. https://doi.org/10.18632/oncotarget.7525

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Abstract

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

Correspondence to:

Bing-Hua Jiang, e-mail: [email protected] and [email protected]

Linlin Zhen, e-mail: [email protected]

Keywords: BEAS-2B cells, miR-222, PTEN, ARID1A, tumor growth

Received: September 26, 2015     Accepted: January 14, 2016     Published: February 20, 2016

ABSTRACT

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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