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

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.

• Authors: 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, Bing-Hua Jiang
• Journal: Oncotarget (Oncotarget) Vol. 7 Issue 14 Pg. 17805-14 (Apr 05 2016) ISSN: 1949-2553 [Electronic] United States
• PMID: 26909602 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• MIRN222 microRNA, human
• MicroRNAs
• PTEN Phosphohydrolase
• PTEN protein, human
• Arsenic

Topics

• Animals
• Apoptosis (drug effects)
• Arsenic (toxicity)
• Arsenic Poisoning (pathology)
• Cell Line, Transformed
• Cell Line, Tumor
• Cell Proliferation (drug effects)
• Cell Transformation, Neoplastic (chemically induced)
• Human Umbilical Vein Endothelial Cells
• Humans
• Lung Neoplasms (chemically induced, metabolism, pathology)
• Mice
• Mice, Inbred BALB C
• Mice, Nude
• MicroRNAs (antagonists & inhibitors, biosynthesis, metabolism)
• PTEN Phosphohydrolase (genetics, metabolism)
• Respiratory Mucosa (drug effects, pathology)
• Up-Regulation