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National Institute of Environmental Health Sciences

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Your Environment. Your Health.

Publication Detail

Title: Suppression of miR-143 contributes to overexpression of IL-6, HIF-1α and NF-κB p65 in Cr(VI)-induced human exposure and tumor growth.

Authors: Wang, Lin; Qiu, Jian-Ge; He, Jun; Liu, Wen-Jing; Ge, Xin; Zhou, Feng-Mei; Huang, Ying-Xue; Jiang, Bing-Hua; Liu, Ling-Zhi

Published In Toxicol Appl Pharmacol, (2019 09 01)

Abstract: Hexavalent chromium [Cr(VI)] is a known occupational and environmental contaminant and carcinogen, but new mechanisms of Cr(VI)-induced carcinogenesis remain to be elucidated. In this study, we found that expression of miR-143 is decreased, whereas that of Interleukin 6 (IL-6) is increased in blood samples of Cr(VI)-exposing workers compared with corresponding unexposed workers. In addition, IL-6 was increased in human bronchial epithelial cells (BEAS-Cr) exposed to Cr(VI) compared with unexposed BEAS-2B cells. To further investigate the mechanisms by which Cr(VI) promotes these changes, we assessed the effects of miR-143 on gene expression and found that miR-143 suppressed expression of IL-6, HIF-1α and NF-κB p65, and that inhibiting miR-143 promoted expression of IL-6, HIF-1α and NF-κB p65. Interestingly, IL-6 regulated expression of HIF-1α, and HIF-1α transcriptionally regulated expression of IL-6. Experiments in animals showed that miR-143 inhibited tumor growth and angiogenesis by regulating IL-6/HIF-1α and downstream signaling pathways in vivo. These outcomes support the hypothesis that the miR-143/IL-6/HIF-1α pathway functions to regulate Cr(VI)-induced carcinogenesis.

PubMed ID: 31152816 Exiting the NIEHS site

MeSH Terms: Animals; Bronchi/drug effects; Carcinogenesis/drug effects; Carcinogenesis/genetics; Cell Line; Cell Proliferation/drug effects*; Cell Transformation, Neoplastic/drug effects; Cell Transformation, Neoplastic/genetics; Chromium/adverse effects*; Epithelial Cells/drug effects; Epithelial Cells/metabolism; Female; Gene Expression Regulation/drug effects; Gene Expression Regulation/genetics; Humans; Hypoxia-Inducible Factor 1, alpha Subunit/genetics*; Interleukin-6/genetics*; Lung Neoplasms/genetics; Mice; Mice, Inbred BALB C; Mice, Nude; MicroRNAs/genetics*; NF-kappa B/genetics; Reactive Oxygen Species/metabolism; Signal Transduction/drug effects; Transcription Factor RelA/genetics*

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