Leptin Promotes Prostate Cancer Proliferation and Migration by Stimulating STAT3 Pathway
Leptin Promotes Prostate Cancer Proliferation and Migration by Stimulating STAT3 Pathway
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DOI：
10.1080/01635581.2020.1792946
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发表时间：
2020-07-22
影响因子：
2.9
通讯作者：
Gati, Asma
中科院分区：
文献类型：
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作者：
Gorrab, Amal;Pagano, Alessandra;Gati, Asma
为了更好地了解肥胖与前列腺癌（PC）侵袭性之间的联系，我们研究了肥胖相关脂肪因子瘦素及其受体（Ob-R）在PC细胞迁移中的作用。迁移试验（伤口愈合）用于研究瘦素对DU-145和PC 3细胞系的影响。通过Western Blot进行STAT 3活化。采用荧光显微镜研究了PC和良性前列腺增生（BPH）活检组织中E-cadherin的表达，并通过RT-PCR评估了Ob-R的表达。在本研究中，我们证明高剂量的瘦素通过刺激STAT 3通路促进PC细胞迁移和EMT转变。此外，我们报告说，虽然Ob-R mRNA表达的ADK和BPH切除活检，ADK患者观察到显着更高的水平。最后，我们发现Ob-R mRNA表达与PC预后不良呈正相关。更好地了解瘦素信号传导的分子过程对于确定治疗肥胖相关PC患者的适当方法至关重要。
To better understand the link between obesity and prostate cancer (PC) aggressiveness, we investigate the role of leptin, an obesity associated adipokine, and its receptor (Ob-R) in PC cells migration. The migration assay (Wound-healing) was used to study the leptin impact on DU-145 and PC3 cells lines. STAT3 activation was performed by Western Blot. E-cadherin expression was studied using fluorescence microscopy and Ob-R expression in PC and benign prostatic Hyperplasia (BPH) biopsies was assessed by RT-PCR. In this study we demonstrate that high dose of leptin promotes PC cells migration and EMT transition via the stimulation of STAT3 pathway. In addition, we report that although Ob-R mRNA is expressed by ADK and BPH resections biopsies, significant higher levels were observed for ADK patients. Finally, we found a positive association between Ob-R mRNA expression and worse PC prognosis. A better understanding of the molecular processes of leptin signaling is crucial for identifying appropriate approaches for treatment of obesity-related PC patients.