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Genetic polymorphisms in leptin, adiponectin and their receptors affect risk and aggressiveness of prostate cancer: evidence from a meta-analysis and pooled-review

Journal

ONCOTARGET
Volume 7, Issue 49, Pages 81049-81061

Publisher

IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.12747

Keywords

leptin; adiponectin; prostate cancer; genetic polymorphism; meta-analysis

Funding

  1. National Natural Science Foundation of China [81272835]
  2. Outstanding Talents Cultivation Project of Shanghai Medical System [XBR2013092]
  3. Talents Development Foundation of Shanghai [201302]
  4. Scientific Research Innovation Project of Shanghai Education Committee [14ZZ010]

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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.

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