MCM7 amplification and overexpression promote cell proliferation, colony formation and migration in esophageal squamous cell carcinoma by activating the AKT1/mTOR signaling pathway

• DOI: 10.3892/or.2017.5614
• Publication Date: 2017-05-02T08:48:00Z
• Authors: Yun-Tan Qiu; Wen-Jun Wang; Bing Zhang; Li-Li Mei; Zhi-Zhou Shi
• Keywords: 0301 basic medicine; 0303 health sciences; Esophageal Neoplasms; Stem Cells; TOR Serine-Threonine Kinases; Cyclin-Dependent Kinase 2; Gene Amplification; Minichromosome Maintenance Complex Component 7; Gene Expression Regulation, Neoplastic; 03 medical and health sciences; Cell Movement; Cell Line, Tumor; Gene Knockdown Techniques; Carcinoma, Squamous Cell; Humans; Cyclin D1; Esophageal Squamous Cell Carcinoma; RNA, Small Interfering; Proto-Oncogene Proteins c-akt; Cell Proliferation

The roles and mechanisms of mini-chromosome maintenance complex component 7 (MCM7) amplification overexpression in esophageal carcinogenesis were investigated. By analyzing the TCGA datasets, we found that MCM7 was amplified approximately 12% squamous cell carcinomas (ESCCs), more than 4% head neck stomach carcinomas. Overexpression further verified three independent GEO datasets cancer. Knockdown using two siRNAs significantly inhibited proliferation, colony formation migration KYSE510 EC9706 cells vitro. Noteworthy, silencing suppressed phosphorylation AKT1 mTOR both cells, reduced cycle regulatory proteins cyclin D1, E2 CDK2. Taken together, our findings suggested promoted tumor ESCC via activating AKT1/mTOR signaling pathway.