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Leptin Promotes Prostate Cancer Proliferation and Migration by Stimulating STAT3 Pathway.

Abstract
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.
AuthorsAmal Gorrab, Alessandra Pagano, Khouloud Ayed, Mohamed Chebil, Amine Derouiche, Hervé Kovacic, Asma Gati
JournalNutrition and cancer (Nutr Cancer) Vol. 73 Issue 7 Pg. 1217-1227 ( 2021) ISSN: 1532-7914 [Electronic] United States
PMID32698628 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • LEP protein, human
  • LEPR protein, human
  • Leptin
  • Receptors, Leptin
  • STAT3 Transcription Factor
  • STAT3 protein, human
Topics
  • Cell Line, Tumor
  • Cell Movement
  • Cell Proliferation
  • Humans
  • Leptin (pharmacology)
  • Male
  • Prostatic Neoplasms (pathology)
  • Receptors, Leptin (genetics)
  • STAT3 Transcription Factor (genetics)

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