Dutta Deep, Ghosh Sujoy, Pandit Kaushik, Mukhopadhyay Pradip, Chowdhury Subhankar
Department of Endocrinology and Metabolism, Institute of Post Graduate Medical Education and Research Kolkata, Kolkata, India.
Indian J Endocrinol Metab. 2012 Dec;16(Suppl 3):S596-600. doi: 10.4103/2230-8210.105577.
Leptin, a product of Ob gene from adipocytes regulates appetite, energy expenditure and body mass composition by decreasing orexigenic and increasing anorexigenic neuropeptide release from hypothalamus. Research over the past few years have suggested leptin/leptin receptor dysregulation to have a role in the development of a large variety of malignancies like breast ca, thyroid ca, endometrial ca and gastrointestinal malignancies, predominantly through JAK/STAT pathway which modulates PI3K/AKT3 signaling, ERK1/2 signaling, expression of antiapoptotic proteins (like XIAP), systemic inflammation (TNF-α, IL6), angiogenic factors (VEGF) and hypoxia inducible factor-1a (HIF-1a) expression. In this review, the current understanding of leptin's role in carcinogenesis has been elaborated. Also a few agents modulating leptin signaling to inhibit cancer cell growth has been described.
瘦素是脂肪细胞中Ob基因的产物，它通过减少下丘脑促食欲神经肽的释放和增加抑食欲神经肽的释放来调节食欲、能量消耗和身体成分。过去几年的研究表明，瘦素/瘦素受体失调在多种恶性肿瘤的发生发展中起作用，如乳腺癌、甲状腺癌、子宫内膜癌和胃肠道恶性肿瘤，主要是通过调节PI3K/AKT3信号传导、ERK1/2信号传导、抗凋亡蛋白（如XIAP）表达、全身炎症（TNF-α、IL6）、血管生成因子（VEGF）和缺氧诱导因子-1α（HIF-1α）表达的JAK/STAT途径。在这篇综述中，阐述了目前对瘦素在致癌作用中作用的理解。还描述了一些调节瘦素信号传导以抑制癌细胞生长的药物。
