乳腺癌
脂肪组织
肿瘤微环境
脂肪因子
癌症研究
转移
癌症
医学
串扰
内科学
癌细胞
生物
内分泌学
肥胖
胰岛素抵抗
物理
光学
作者
Xiaodan Lyu,Qian Zhang,Hamza M. Fares,Yifan Wang,Yi Han,Li Sun
出处
期刊:Cancer Letters
[Elsevier]
日期:2022-03-03
卷期号:534: 215616-215616
被引量:17
标识
DOI:10.1016/j.canlet.2022.215616
摘要
Breast cancer is considered the most common malignancy, with the profound ability to perform a wide range of metabolic reprogramming. Within the breast cancer microenvironment, highly available cancer-associated adipocytes interact with cancer cells by releasing various adipocytokines and metabolites. Obesity is also an important factor in this manner, where the accumulation of adipose tissue next to tumor tissue is linked to the increased incidence, progression, and metastasis of breast cancer. The metabolic changes caused by the crosstalk between breast cancer cells and dysfunctional adipose tissue include glucose, lipid, and amino acid metabolism. Thus, preventing this interaction between breast cancer cells and dysfunctional adipose tissue might develop a promising therapeutic strategy against breast cancer. This review focused on the metabolic changes responsible for inducing the crosstalk between breast cancer cells and adipocytes. We also reviewed the recent updates in therapeutics designed to disrupt this interaction.
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