Abstract
Long-term heavy cigarette smoking is a well-known high-risk factor for carcinogenesis in various organs such as the head and neck, lungs, and urinary bladder. Furthermore, cigarette smoking can systemically accelerate aging, and as the result, promoting carcinogenesis via changing the host microenvironment. Various inflammatory factors, hormones, and chemical mediators induced by smoking mediate carcinoma-related molecules and induce carcinogenesis. MicroRNAs (miRNAs) are a family of short noncoding RNA molecules that bind to mRNAs and inhibit their expression. Cigarette smoke induces the expression of various miRNAs, many of which are known to function in the post-transcriptional silencing of anticancer molecules, thereby leading to smoking-induced carcinogenesis. Analysis of expression profiles of smoking-induced miRNAs can help identify biomarkers for the diagnosis and prognosis of smoking-related cancers and prediction of therapeutic responses, as well as revealing promising therapeutic targets. Here, we introduce the most recent and useful findings of miRNA analyses focused on lung cancer and urinary bladder cancer, which are strongly associated with cigarette smoking, and discuss the utility of miRNAs as clinical biomarkers.
Highlights
Cigarette smoking has been proposed as the cause of various cancers, including lung, urinary system and bladder, head and neck, liver, esophagus, pancreas, and oral cancer [1,2]
In vitro experimental model systems for miRNA alterations mediated by cigarette smoking in normal human bronchial epithelial and lung cancer cells derived from smokers and nonsmokers have demonstrated the repression of miR-487b, which leads to the upregulation of suppressor of zest 12 (SUZ12), B cell-specific Moloney murine leukemia virus insertion site 1 (BMI1), wingless-type family member 5A (WNT5A), MYC, and KRAS, thereby increasing cell proliferation, invasion, tumorigenicity, and metastatic potential of lung cancer cells in the cigarette-smoking group [14]
Various genes have been associated with the neoplastic transformation of respiratory epithelium by cigarette smoking. miRNAs play an important role in the regulation of genes involved in carcinogenesis and cancer progression, such as those involved in autophagy and cell senescence
Summary
Cigarette smoking has been proposed as the cause of various cancers, including lung, urinary system and bladder, head and neck, liver, esophagus, pancreas, and oral cancer [1,2]. In vitro experimental model systems for miRNA alterations mediated by cigarette smoking in normal human bronchial epithelial and lung cancer cells derived from smokers and nonsmokers have demonstrated the repression of miR-487b, which leads to the upregulation of suppressor of zest 12 (SUZ12), B cell-specific Moloney murine leukemia virus insertion site 1 (BMI1), wingless-type family member 5A (WNT5A), MYC, and KRAS, thereby increasing cell proliferation, invasion, tumorigenicity, and metastatic potential of lung cancer cells in the cigarette-smoking group [14]. In females, smokers have a higher risk for epidermal growth factor receptor (EGFR) mutations (exons 18, 19, and 21) compared to nonsmokers These findings suggest that the histological type is closely associated with the mechanism of action of smoking-related carcinogens. Detailed information of the smoking history allows us to select biomarkers and the most useful cancer therapy
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