RESUMEN
BACKGROUND: Metabolic syndrome (MetS) has been related to the increased incidence of esophageal cancer (EC). The aim of the study was to evaluate the influence of MetS on prognosis of patients with surgically treated EC in a systematic review and meta-analysis. METHODS: An extensive search was conducted on PubMed, Embase, Web of Science, Wanfang, and CNKI to identify relevant cohort studies. Random-effects models were employed to combine the findings, taking into account the potential influence of heterogeneity. RESULTS: Seven cohort studies involving 4332 patients with stage I-III EC who received surgical resection were included. At baseline, 608 (14.0%) patients had MetS. Pooled results suggested that MetS were associated with a higher risk of postoperative complications (risk ratio [RR]: 1.30, 95% confidence interval [CI]: 1.03 to 1.64, p = 0.03; I2 = 0%). However, the overall survival (RR: 1.07, 95% CI: 0.75 to 1.52, p = 0.71; I2 = 80%) and progression-free survival (RR: 1.27, 95% CI: 0.53 to 3.00, p = 0.59; I2 = 80%) were not significantly different between patients with and without MetS. Subgroup analyses suggested that the results were not significantly modified by study design (prospective or retrospective), histological type of EC (squamous cell carcinoma or adenocarcinoma), or diagnostic criteria for MetS (p values indicating subgroup difference all > 0.05). CONCLUSION: Although MetS may be associated with a moderately increased risk of postoperative complications in patients with EC under surgical resection, the long-term survival may not be different between patients with and without MetS.
RESUMEN
Polo-like kinase 3 (Plk3) is involved in tumor development with a tumor suppressive function. However, the effect of Plk3 on the chemoresistance remains unclear. It has been documented that activation of the PI3K/AKT signaling pathway by PTEN loss significantly enhances chemoresistance in nonsmall-cell lung cancer (NSCLC). This study aims to evaluate the PTEN regulation by Plk3 and identify targets and underlying mechanisms that could be used to relieve chemoresistance. Our results showed that silencing Plk3 reduced PTEN expression and activated PI3K/AKT signaling by dephosphorylating and destabilizing PTEN in NSCLC cells. Reducing Plk3 expression promoted drug resistance to cisplatin (DDP), while overexpressing Plk3 promoted DDP sensitivity. However, these effects were attenuated when MK2206, a PI3K/AKT inhibitor, was applied. In conclusion, upregulation of Plk3 sensitized NSCLC cells toward DDP, which provides a potential target to restore DDP chemoresponse. We provided novel evidence that the PTEN/PI3K/AKT signaling pathway could be regulated by Plk3 through phosphorylation of PTEN and highlighted the critical role of Plk3 in the DDP resistance of NSCLC.
