1. Lipid Metabolism Fuels Cancer’s Spread
Zhuo Li, Yibin Kang 
Cell Metabolism 
Volume 25, Issue 2, Pages (February 2017)
DOI: /j.cmet
Copyright © 2017 Elsevier Inc. Terms and Conditions

2. Figure 1
A Metastasis-Initiating Cancer Cell Population, Marked by the Expression of Fatty Acid Receptor CD36, Drives Metastasis in a Lipid Metabolism-Dependent Manner
CD36 is expressed at high levels in many metastatic tumors, such as oral squamous cell carcinomas (OSCC), melanoma, and breast cancers. In OSCC, among CD44bright tumor-initiating cells (TICs) exist a unique CD36+ population of metastasis-initiating cells (MICs) that have higher propensity to metastasize to lymph nodes and lungs compared to their CD36− counterparts. CD36 promotes fatty acid uptake and lipid metabolism, which is critical for metastatic colonization in distant organs (upper panel). Inhibition of CD36—either by (1) short hairpin RNA (shRNA)-mediated knockdown, (2) administration of neutralizing antibodies, or (3) expression of a CD36 mutant that cannot internalize fatty acids—significantly reduces the formation of metastases without causing significant adverse side effects in preclinical models (lower panel). Mechanistically, CD36 depletion or inhibition leads to impaired lipid metabolism and continuous accumulation of lipid droplets in tumor cells, eventually resulting in lipotoxicity and cell death.
Cell Metabolism  , DOI: ( /j.cmet )
Copyright © 2017 Elsevier Inc. Terms and Conditions