作者: JIAN GONG , YI CHU , MEILI XU , JIRONG HUO , LIANG LV
DOI: 10.3892/OR.2015.4379
关键词:
摘要: Cigarette smoke has been implicated as a major risk factor for esophageal squamous cell carcinoma (ESCC). Several lines of evidence have suggested that the promoting effect cigarette smoking extract (CSE) on ESCC is mediated by upregulation cyclooxygenase-2 (COX-2) expression. Yet, underlying molecular and cellular mechanisms how CSE stimulates COX-2 expression facilitates development are largely unknown. In present study, we revealed microRNA (miR)-101-3p was downregulated upon exposure to low concentration in Eca109 cancer cells, suppression miR-101-3p required CSE-induced proliferation, presenting overexpression reversing stimulated growth. Luciferase assay direct target decreased protein Furthermore, found inhibitor knockdown siRNA interference could abolish indicating promotion proliferation dependent activity. Finally, downregulation specimens from patients with history. Taken together, our findings new post-transcriptional mechanism which regulated favor suggesting potential biomarker therapeutic smoke-related ESCC.