RACK1 promotes lung cancer cell growth via an MCM7/RACK1/Akt signaling complex
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Liangru Fei1, Yinan Ma1, Meiyu Zhang1, Xiaofang Liu2, Yuan Luo1, Congcong Wang2, Haiyan Zhang3, Wenzhu Zhang1 and Yuchen Han1,2
1Department of Pathology, School of Basic Medical Sciences, China Medical University, Shenyang 110000, China
2Department of Pathology, The First Affiliated Hospital of China Medical University, Shenyang 110000, China
3Department of Pathology, The First People’s Hospital of Jining, Shandong 272000, China
Yuchen Han, email: email@example.com
Keywords: RACK1, MCM7, proliferation, NSCLC, Akt
Received: December 16, 2016 Accepted: April 03, 2017 Published: April 15, 2017
MCM7, a member of the miniature chromosome maintenance (MCM) protein family, is crucial for the initiation of DNA replication and proliferation in eukaryotic cells. In this report, we demonstrate that RACK1 regulates cell growth and cell cycle progression in human non-small-cell lung cancer by mediating MCM7 phosphorylation through an MCM7/RACK1/Akt signaling complex. RACK1 functions as a central scaffold that brings Akt into physical proximity with MCM7. Overexpression of RACK1 increases interactions between Akt and MCM7 and promotes Akt-dependent MCM7 phosphorylation, which in turn increases MCM7 binding to chromatin and MCM complex formation. Together, these changes promote DNA replication and cell proliferation. Our findings reveal a novel signaling pathway that regulates growth in non-small cell lung cancer.
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