Hu Meng-Bo, Xu Hua, Hu Ji-Meng, Zhu Wen-Hui, Yang Tian, Jiang Hao-Wen, Ding Qiang
Department of Urology, Huashan Hospital, Fudan University, Shanghai 200040, China.
Oncotarget. 2016 Dec 6;7(49):81049-81061. doi: 10.18632/oncotarget.12747.
Leptin and adiponectin signaling was associated with development and progression of various cancers. The present study aimed to clarify the role of genetic variants in leptin, adiponectin and their receptors in prostate cancer. After comprehensive search and manuscript scanning, a total of 49 genetic variants were enrolled and examined for their relations to cancer risk and aggressiveness. In the meta-analysis, LEP rs7799039 (allele contrast: OR 1.133, 95%CI 1.024-1.254), ADIPOQ rs2241766 (allele contrast: OR 1.201, 95%CI 1.015-1.422) and ADIPOR1 rs10920531 (allele contrast: OR 1.184, 95%CI 1.075-1.305) variants were identified to be correlated with increased risk of prostate cancer. On the contrary, LEPR rs1137101 (allele contrast: OR 0.843, 95%CI 0.730-0.973) and ADIPOR1 rs2232853 (allele contrast: OR 0.638, 95%CI 0.535-0.760) variants were associated with decreased risk of prostate cancer. From the pooled-review, we additionally recognized eight variants associated with cancer risk and another eight variants associated with cancer aggressiveness, respectively. These observations indicated important roles of leptin, adiponectin and their receptors in the development and progression of prostate cancer. The identified polymorphisms might assist in developing better risk-assessment tools, as well as generating novel targeted therapies, especially for obese cancer patients with impaired leptin and adiponectin signaling.
瘦素和脂联素信号传导与多种癌症的发生和发展相关。本研究旨在阐明瘦素、脂联素及其受体的基因变异在前列腺癌中的作用。经过全面检索和文献筛选,共纳入49个基因变异,并检测它们与癌症风险和侵袭性的关系。在荟萃分析中,发现LEP rs7799039(等位基因对比:OR 1.133,95%CI 1.024 - 1.254)、ADIPOQ rs2241766(等位基因对比:OR 1.201,95%CI 1.015 - 1.422)和ADIPOR1 rs10920531(等位基因对比:OR 1.184,95%CI 1.075 - 1.305)变异与前列腺癌风险增加相关。相反,LEPR rs1137101(等位基因对比:OR 0.843,95%CI 0.730 - 0.973)和ADIPOR1 rs2232853(等位基因对比:OR 0.638,95%CI 0.535 - 0.760)变异与前列腺癌风险降低相关。通过汇总分析,我们还分别识别出另外八个与癌症风险相关的变异和八个与癌症侵袭性相关的变异。这些观察结果表明瘦素、脂联素及其受体在前列腺癌的发生和发展中起重要作用。所确定的多态性可能有助于开发更好的风险评估工具,以及产生新的靶向治疗方法,特别是对于瘦素和脂联素信号传导受损的肥胖癌症患者。