Research Papers:

MiR-495 inhibits esophageal squamous cell carcinoma progression by targeting Akt1

Yu Mao _, Liang Li, Jia Liu, Le Wang and Yan Zhou

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Oncotarget. 2016; 7:51223-51236. https://doi.org/10.18632/oncotarget.9981

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Yu Mao1, Liang Li2, Jia Liu3, Le Wang4, Yan Zhou5

1Department of Oncology, The First Hospital of Qinhuangdao, Qinhuangdao, Hebei, China

2Department of Ultrasound, Beijing Anzhen Hospital, Capital Medical University, Beijing, China

3Institute of Basic Medical Sciences, Qilu Hospital, Shandong University, Jinan, China

4Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin Neurological Institute and Laboratory of Neuro -Oncology, Tianjin, China

5Department of Radiotherapy, Tianjin General Hospital, Tianjin, China

Correspondence to:

Yu Mao, email: [email protected]

Keywords: miR-495, esophageal squamous cell carcinoma, progression, Akt1

Received: October 19, 2015     Accepted: May 20, 2016     Published: June 13, 2016


MicroRNAs are involved in tumor initiation and progression by regulating oncogenes and tumor suppressor genes. Here we found that miR-495 are lower in clinical ESCC tissues than in adjacent non-tumor tissues. Moreover, the lower miR-495 expression correlated with increased lymph node metastasis (LNM), invasion and TNM stage. miR-495 overexpression predicted a favorable outcome in ESCC patients. miR-495 targeted a site in the 3’-UTR of Akt1, and miR-495 levels correlated inversely with Akt1 protein levels in ESCC tissue samples. Overexpression of miR-495 suppressed cell proliferation, blocked G1/S phase transition, and decreased migration and invasion by two ESCC cell lines in vitro and in vivo. Restoration of Akt1 protein levels in miR-495-overexpressing ESCC cells attenuated the inhibitory effects of miR-495. In addition, miR-495 suppressed cell cycle transition and the EMT signaling pathway through targeting Akt1, thereby inhibiting ESCC cell proliferation, migration, and invasion. Our results suggest that miR-495 may act as a tumor suppressor by targeting Akt1 in ESCC.

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