Role of tissue microenvironment resident adipocytes in colon cancer

作     者：Maria Tabuso Shervanthi Homer-Vanniasinkam Raghu Adya Ramesh P Arasaradnam 

作者机构：Department of Gastro-enterologyUniversity Hospitals Coventry and Warwickshire Warwick Medical SchoolUniversity of Warwick Leeds Institute of Car-diovascular and Metabolic MedicineFaulty of Medicine and HealthUniversity of Leeds Division of Surgical and Interventional SciencesUCL Medical School Building Applied Biological and Experimental SciencesUniversity of Coventry 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2017年第23卷第32期

页      面：5829-5835页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

主　　题：Tumour resident adipocytes Dysfunctional adipocytes Adipose tissue Cancer cell-tumour resident adipocyte cross-talk Colon cancer microenvironment 

摘      要：Colorectal cancer(CRC) is a multifactorial disease characterized by several genetic and epigenetic alterations occurring in epithelial cells. It is increasingly recognized that tumour progression is also regulated by tumour microenvironment(TME). The bidirectional cross-talk between tumour resident adipocytes and cancer cells within TME has been proposed as active contributor to carcinogenesis. Tumour resident adipocytes exhibit an activated phenotype characterized by increased secretion of pro-tumorigenic factors(angiogenic/inflammatory/immune) which contribute to cancer cell proliferation, invasion, neoangiogenesis, evasion of immune surveillance and therapy resistance. Furthermore, adipocytes represent a fuel rich source for increasing energy demand of rapidly proliferating tumour cells. Interestingly, a relationship between obesity and molecular variants in CRC has recently been identified. Whether adipose tissue promotes cancer progression in subsets of molecular phenotypes or whether local tissue adipocytes are involved in inactivation of tumour suppressor genes and/or activation of oncogenes still needs to be explored. This editorial highlights the major findings related to crosstalk between adipocytes and colon cancer cells and how local paracrine interactions may promote cancer progression. Furthermore, we provide future strategies in studying colonic TME which could provide insights in bidirectional cross-talk mechanisms between adipocytes and colonic epithelial cells. This could enable to decipher critical signalling pathways of both early colonic carcinogenesis and cancer progression.