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Publication Detail

Title: Arsenic activates STAT3 signaling during the transformation of the human bronchial epithelial cells.

Authors: Almutairy, Bandar; Fu, Yao; Bi, Zhuoyue; Zhang, Wenxuan; Wadgaonkar, Priya; Qiu, Yiran; Thakur, Chitra; Chen, Fei

Published In Toxicol Appl Pharmacol, (2022 Feb 01)

Abstract: Arsenic (As3+), a metalloid abundant in environment, is classified as a group I carcinogen associated with several common human cancers, including cancers in lung, skin, bladder, liver, and prostate (Wei et al., 2019). The mechanisms of As3+-induced carcinogenesis had been extensively studied, and different mechanisms might be involved in different types of cancer (Wei et al., 2019). Recent studies showed that exposure to a high dose of arsenic is able to induce lung cancer. Meanwhile, prolonged exposure to a low concentration of arsenic can increase the risk of lung cancer also (Liao et al., 2009; Fernández et al., 2012). Emerging evidence indicated that prolonged exposure to arsenic promotes malignant transformation and some of the transformed cells have cancer-stem-like properties (Ngalame et al., 2014). In the present report, we revealed that exposure to As3+ for short time period inhibited tyrosine-705 phosphorylation of signal transducer and activator of transcription 3 (pSTAT3Y705) and induced Src homology region 2 domain-containing phosphatase-1 (SHP-1) in bronchial epithelial cell line, BEAS-2B. In addition, we found that long term exposure of the cells to As3+ activates phosphorylation of STAT3 at serine 727 (pSTAT3S727) as well as pSTAT3Y705. Moreover, As3+ is able to induce the expression of miRNA-21 (miR-21) and decrease the expression of PDCD4. Taken together, our data suggest that activation of STAT3 and induction of miR-21 are important contributing factors to the reduced expression of PDCD4, which may play significant role in As3+-induced transformation of BEAS-2B cells.

PubMed ID: 35031324 Exiting the NIEHS site

MeSH Terms: Apoptosis Regulatory Proteins/genetics; Arsenic/adverse effects*; Bronchi/drug effects*; Bronchi/metabolism; Carcinogenesis/chemically induced; Carcinogenesis/genetics; Cell Transformation, Neoplastic/drug effects*; Cell Transformation, Neoplastic/genetics; Cells, Cultured; Epithelial Cells/drug effects*; Epithelial Cells/metabolism; Gene Expression Regulation, Neoplastic/drug effects; Gene Expression Regulation, Neoplastic/genetics; Humans; Lung Neoplasms/chemically induced; Lung Neoplasms/genetics; Lung Neoplasms/metabolism; Phosphorylation/drug effects; Phosphorylation/genetics; RNA-Binding Proteins/genetics; Reactive Oxygen Species/metabolism; STAT3 Transcription Factor/genetics*; Signal Transduction/drug effects*; Signal Transduction/genetics

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