Abstract

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a known tumor suppressor in non-small cell lung cancer (NSCLC). By performing a systematic review and meta-analysis of the literature, we determined the prognostic value of decreased PTEN expression in patients with NSCLC. We comprehensively and systematically searched through multiple online databases up to May 22, 2016 for NSCLC studies reporting on PTEN expression and patient survival outcome. Several criteria, including the Newcastle-Ottawa Quality Assessment Scale (NOS), were used to discriminate between studies. In total, 23 eligible studies with a total of 2,505 NSCLC patients were included in our meta-analysis. Our results demonstrated that decreased expression of PTEN correlated with poor overall survival in NSCLC patients and was indicative of a poor prognosis for disease-free survival and progression-free survival in patients with NSCLC.

Highlights

  • Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a protein that can modulate cell survival and cell cycle progression [1]

  • 2,505 nonsmall cell lung cancer (NSCLC) patients were included and the survival data were organized based on overall survival (OS), disease-free survival (DFS) and progression-free survival (PFS)

  • What’s more, we found that decreased expression of PTEN indicated a poor prognosis for DFS and PFS in patients with NSCLC

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Summary

Introduction

Phosphatase and tensin homolog deleted on chromosome 10 (PTEN) is a protein that can modulate cell survival and cell cycle progression [1]. PTEN can control smooth muscle differentiation [2], mediate angiogenesis [3], maintain Treg cell stability [4], and coordinate retinal neurogenesis [5]. PTEN is a tumor suppressor that is commonly down-regulated in many types of cancer [6], including nonsmall cell lung cancer (NSCLC) [7, 8]. Inactivation of PTEN can augment invasiveness and anchorage independent growth of NSCLC cells [9]. In some animal models, PTEN inactivation accelerates tumorigenesis [10]. Exogenously imported PTEN can suppress lung tumorigenesis [11]. PTEN upregulation can inhibit NSCLC cell growth and promote partial apoptosis [12]

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