Abstract
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.
Highlights
Prostate cancer (PCa) recently became the second most frequently diagnosed malignant tumor, and the fifth leading cause of cancer death in men throughout the world [1]
Both leptin and adiponectin relied on binding to their receptors, leptin receptor (LEPR) or adiponectin receptor 1/2 (ADIPOR1/ ADIPOR2), to activate downstream signaling and functioning [13, 14]
The meta-analysis yielded five polymorphisms that associated with PCa risk according to allele contrast model
Summary
Prostate cancer (PCa) recently became the second most frequently diagnosed malignant tumor, and the fifth leading cause of cancer death in men throughout the world [1]. In vitro studies revealed that leptin and its downstream signaling might induce cell proliferation [8], inhibit apoptosis [9], and mediate metabolism [10]. Study showed that adiponectin (ADIPOQ) inhibited proliferation and invasion of PCa cells [11]. The adiponectin level was proved lower in patients with metastatic PCa compared to those with organ-confined diseases [12]. Both leptin and adiponectin relied on binding to their receptors, leptin receptor (LEPR) or adiponectin receptor 1/2 (ADIPOR1/ ADIPOR2), to activate downstream signaling and functioning [13, 14]
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