口腔医学研究 ›› 2022, Vol. 38 ›› Issue (1): 24-29.DOI: 10.13701/j.cnki.kqyxyj.2022.01.006

• 口腔肿瘤学研究 • 上一篇    下一篇

MUC1通过调控EGFR/ERK信号通路促进唾液腺腺样囊性癌细胞增殖和侵袭的研究

卢浩, 徐万林, 吴一凡, 朱云, 刘胜文*, 杨雯君   

  1. 上海交通大学医学院附属第九人民医院口腔颌面-头颈肿瘤科;
    上海交通大学口腔医学院;
    国家口腔医学中心;
    国家口腔疾病临床医学研究中心;
    上海市口腔医学重点实验室 上海 200011
  • 收稿日期:2021-07-12 出版日期:2022-01-28 发布日期:2022-01-21
  • 通讯作者: * 刘胜文,E-mail:wubenzhimu@163.com
  • 作者简介:卢浩(1990~ ),男,山东聊城人,住院医师,博士,主要从事唾液腺肿瘤的临床与基础研究。
  • 基金资助:
    上海市青年科技英才扬帆计划资助(编号:20YF1423300);上海市卫健委青年项目(编号:20204Y0456);上海第九人民医院生物样本库项目(编号:YBKB201920)

MUC1 Promotes Growth and Invasion of Salivary Adenoid Cystic Carcinoma Cells via EGFR/ERK Signaling Pathway

LU Hao, XU Wanlin, WU Yifan, ZHU Yun, LIU Shengwen*, Yang Wenjun   

  1. Department of Oral Maxillofacial-Head and Neck Oncology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine;
    College of Stomatology, Shanghai Jiao Tong University;
    National Center for Stomatology;
    National Clinical Research Center for Oral Diseases;
    Shanghai Key Laboratory of Stomatology, Shanghai 200011, China
  • Received:2021-07-12 Online:2022-01-28 Published:2022-01-21

摘要: 目的:研究黏蛋白1(MUC1)对唾液腺腺样囊性癌(ACC)细胞生物学功能的影响及其分子机制。方法:首先通过慢病毒(shMUC1)转染对ACC细胞系中MUC1基因进行敲减,通过Real-time PCR和Western blot检测敲减效果;CCK-8实验检测细胞的增殖能力;平板克隆形成实验评价细胞的克隆形成能力;Transwell实验检测细胞的迁移和侵袭能力;采用转录组测序筛选MUC1调控的相关信号通路,并通过Wesern blot验证分析。结果:转染MUC1慢病毒后,ACC细胞中MUC1 mRNA和蛋白表达量显著降低(P<0.05);MUC1敲减后ACC细胞的增殖、迁移和侵袭能力均显著下降(P<0.05);转录组测序分析和Western blot结果表明MUC1主要通过调控EGFR/ERK磷酸化水平影响ACC细胞的生物学功能。结论:MUC1可通过调控EGFR/ERK磷酸化水平促进ACC细胞的增殖、平板克隆、迁移和侵袭,提示MUC1在ACC进展中可能发挥重要作用。

关键词: 黏蛋白1, 腺样囊性癌, 增殖, 侵袭

Abstract: Objective: To investigate the effects of MUC1 on the biological properties of salivary gland adenoid cystic carcinoma (ACC) cells and the underlying mechanisms. Methods: MUC1 silenced ACC cell line was constructed by lentivirus. Real-time PCR and western blotting were performed to evaluate the efficiency of MUC1 knock-down. CCK-8 assay was used to detect cell proliferation and plate colony assay was carried out to detect cell clone formation ability. Transwell assays were utilized to investigate cell migration and invasion ability. RNA-seq analysis was used to explore the molecular mechanisms regulated by MUC1. Results: MUC1 was knocked down in SACC cell by shRNA. The down-regulation of MUC1 attenuated the proliferation, migration, and invasion ability of SACC cells. RNA-seq analysis and western blot assay showed that MUC1 could regulate biological effects of SACC cells mainly via EGFR/ERK signaling pathway. Conclusion: MUC1 plays a crucial role in regulating ACC cell biological behaviors by regulating phosphorylation levels of EGFR/ERK and may play a role in the development of ACC.

Key words: Mucin1, salivary adenoid cystic carcinoma, proliferation, invasion