Research progress on role of LncRNAs in tumorigenesis in arsenic-exposed population
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Abstract
Inorganic arsenic (iAs) is a widespread environmental toxicant that has been classified as a human carcinogen by the International Agency for Research on Cancer. It is associated with increased risks of bladder, lung, and breast cancer via a variety of ways. How arsenic exposure promotes diseases remains unclear. Researchers have explored the genotoxicity and carcinogenic mechanisms of arsenic from many aspects, and have found significant changes in the expression of long non-coding RNAs (LncRNAs) in occupational arsenic-exposed population, indicating potential risk for cancer initiation. This article reviewed various metabolic patterns of arsenic methylation and associated contents and proportions of its metabolites, as well as the role of abnormal expression of LncRNAs induced by arsenic in tumors. LncRNAs as proto-oncogenes (MALAT1 and HOTAIR for example) in arsenic-exposed population can promote tumor initiation by coordinating hypoxia inducible factors and transcription factor nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway; as antioncogenes (MEG3 and LincRNA-p21 for example) they can inhibit the proliferation and invasion of cancer cells; they also participate in the co-regulation of tumorigenesis with competing endogenous RNA or p53 network. The article aimed to provide new ideas for screening high-risk population with arsenic exposure and for the early diagnosis and treatment of related diseases.
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