瘦素
脂肪因子
前列腺癌
增生
车站3
癌症研究
免疫印迹
小鼠苗条素受体
医学
内科学
内分泌学
癌症
化学
生物
肥胖
信号转导
细胞生物学
基因
生物化学
作者
Gorrab Amal,Alessandra Pagano,Khouloud Ayed,Mohamed Chébil,A. Derouiche,Hervé Kovacic,Asma Gati
标识
DOI:10.1080/01635581.2020.1792946
摘要
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.
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