[No authors listed]
Cigarette smoking is a factor capable of inducing esophageal squamous cell carcinoma (ESCC). However, the biological pathways that are responsible for tumor development and are directly affected by cigarette smoking remain unknown. To explore the role of cigarette smoking in ESCC, we developed a long-term cigarette smoke extract (CSE) exposed cell model using the normal immortalized SHEE esophageal epithelial cell line, which would malignantly transform after long-term cultivation without carcinogens. CSE-exposed cells displayed higher malignancy and differently expressed several lncRNAs. Among them, H19, a lncRNA responsible for proliferation and invasion, was upregulated in CSE-exposed SHEE cells. In tumors from ESCC patients, H19 was significantly increased in smoking ESCC patients compared to non-smoking patients, and H19 was overexpressed and correlated with pathological tumor size in smokers. These results indicated that cigarette smoking lead to a different biological change from non-smoking induced ESCC and H19 related to cancer development during CSE-induced carcinogenesis.
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