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.
Highlights
Long-term exposure to arsenic can result in skin, liver, lung, and other types of cancer [1,2,3]
The result showed that cell migration was decreased by more than 2-fold in As-T cells transfected with anti-miR-222 inhibitor (Figure 2E)
We focus on the role and mechanism of miR-222 in mediating tumorigenesis using transformed cells through chronic arsenite exposure
Summary
Long-term exposure to arsenic can result in skin, liver, lung, and other types of cancer [1,2,3]. MiRNAs may play roles as tumor suppressors or oncogenes through their targets. MiR-199a and miR-145 are commonly regarded as tumor suppressor genes in many cancers [7, 8]. MiR-222 can increase migration and proliferation of tumor cell, and inhibit apoptosis by regulating different targets such as PTEN [9], p27 [10], and TIMP3 [11]. Overexpression of miR-222 is correlated with the poor prognosis of nonsmall cell lung cancer (MSCLC) and miR-122 may be used as a biomarker for selecting the Tube formation assay patients who require especial attention [12]
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