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학술저널
저자정보
Xiaopeng Guo (Department of Otorhinolaryngology-Head and Neck Surgery Affiliated Hospital of Guizhou Medical University Guiyang China) Xianlu Zhuo (Department of Otorhinolaryngology-Head and Neck Surgery Affiliated Hospital of Guizhou Medical University Guiyang China) Zhen Sun (Department of Otorhinolaryngology-Head and Neck Surgery Affiliated Hospital of Guizhou Medical University Guiyang China) Huarong Chen (Department of Otorhinolaryngology-Head and Neck Surgery Affiliated Hospital of Guizhou Medical University Guiyang China) Junjun Ling (Department of Otorhinolaryngology-Head and Neck Surgery Affiliated Hospital of Guizhou Medical University Guiyang China) Houyu Zhao (Department of Otorhinolaryngology-Head and Neck Surgery Affiliated Hospital of Guizhou Medical University Guiyang China) Aoshuang Chang (Department of Otorhinolaryngology-Head and Neck Surgery Affiliated Hospital of Guizhou Medical University Guiyang China)
저널정보
대한이비인후과학회 Clinical and Experimental Otorhinolaryngology Clinical and Experimental Otorhinolaryngology 제16권 제1호
발행연도
2023.2
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75 - 86 (12page)

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Objectives. Nicotine is an ingredient of tobacco, and exposure to nicotine increases the risks of various cancers, includingoral cancer. Previous studies have focused on the addictive properties of nicotine, but its carcinogenic mechanism hasrarely been studied. We aimed to explore the key genes in the process through which nicotine promotes the occur-rence and development of oral cancer via data mining and experimental verification. Methods. This study involved three parts. First, key genes related to nicotine-related oral cancer were screened throughdata mining; second, the expression and clinical significance of a key gene in oral cancer tissues were verified by bio-informatics. Finally, the expression and clinical significance of the key gene in oral cancer were histologically investi-gated, and the effects of its expression on cell proliferation, invasion, and drug resistance were cytologically assessed. Results. SERPINE1 was identified as the key gene, which was upregulated in nicotine-treated oral cells and may be an in-dependent prognostic factor for oral cancer. SERPINE1 was enriched in various pathways, such as the tumor necro-sis factor and apelin pathways, and was related to the infiltration of macrophages, CD4+T cells, and CD8+T cells. Overexpression of SERPINE1 was associated with N staging and may be involved in hypoxia, angiogenesis, and me-tastasis. Knockdown of SERPINE1 in oral cancer cells resulted in weakened cell proliferation and invasion abilityand increased sensitivity to bleomycin and docetaxel. Conclusion. This study revealed SERPINE1 as a key gene for nicotine-related oral cancer, indicating that SERPINE1 maybe a novel prognostic indicator and therapeutic target for oral carcinoma.

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