Oncotarget · 2017 · 43 citations · 38 references
MedicineMolecular BiologyOncologyCarcinogenesisGene ExpressionMolecular OncologyCancer Cell SignalingOncogenic Signaling PathwaysSignal Transduction In CancerTumor Suppressor Gene InactivationTumor Suppressor GenesAnticancer ActivityCancer Cell Proliferation InhibitionLung Cancer PathologyMicrorna Function In CancerMicrorna In CancerMicrorna ModulationPten Inactivation
// Zhaoming Li 1 , Ran Qiu 2 , Xia Qiu 3 and Tian Tian 4 1 Department of Oncology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China 2 Wuhan Institute of Bioengineering, Wuhan, China 3 Department of Medicine, Shangqiu Medical School, Shangqiu, China 4 Department of Neurology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China Correspondence to: Tian Tian, email: zhaomingli2008@hotmail.com Keywords: EYA2; PTEN; lung cancer; cell proliferation; prognosis Received: September 04, 2017 Accepted: October 29, 2017 Published: December 02, 2017 ABSTRACT Lung cancer is the leading cause of cancer-related death worldwide. Despite advances have been made in diagnosis and therapeutic strategies, the prognosis of lung cancer is still very poor. Eyes absent transcriptional cofactor EYA2 has been shown to promote lung cancer cell growth, however, the underlying molecular mechanism is still not fully understood. In the present study, we found that EYA2 was up-regulated in lung cancer, and EYA2 led to increased cell proliferation by inhibiting Phosphatase and tensin homologue (PTEN) expression via modulation of miR-93. Additionally, survival analysis showed that lung cancer patients with higher EYA2 expression predicted a worse prognosis. Therefore, these findings demonstrate that EYA2 may play an important role in lung cancer occurrence and progression. Targeting EYA2 may provide a feasible approach in developing novel anticancer therapeutics.
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