Prothymosin α promotes colorectal carcinoma chemoresistance through inducing lipid droplet accumulation

Colorectal cancer (CRC) affects millions of people worldwide. Chemoresistance seriously impairs the therapeutic effects. Lipid droplets (LDs) abnormally accumulate in CRC supported chemoresistance. Exploring the mechanism of LD-induced chemoresistance is extremely important for improving prognosis of CRC patients. The expression of PTMA was increased in both CRC tissues and cells, which was positively correlated with LD production. PTMA facilitated chemoresistance to gemcitabine by inducing LD production in CRC cells. PTMA enhanced LD biogenesis and chemoresistance to gemcitabine by promoting SREBP-1-mediated lipogenesis and STAT3 activation in CRC.

Automated summary

The abnormal accumulation of lipid droplets in colorectal cancer (CRC) contributes to chemoresistance, with the expression of PTMA positively correlated with LD production and enhancing resistance to gemcitabine in CRC cells. PTMA promotes LD biogenesis and chemoresistance to gemcitabine by facilitating SREBP-1-mediated lipogenesis and STAT3 activation in CRC.