Genistein inhibits colorectal cancer progression via regulating the LINC00355/miR-150/SGK1 axis and downstream EGFR/PI3K/AKT and MAPK signaling pathways.
TL;DR
This study provides reliable experimental evidence for the development of genistein as a potential adjuvant therapeutic agent for CRC treatment by revealing that genistein dose-dependently inhibited CRC cell proliferation without obvious cytotoxicity to normal colon cells.
Abstract
Colorectal cancer (CRC) is a major global malignant tumor with high morbidity and mortality, and current clinical therapies have limited curative effects and obvious adverse reactions. Genistein, a key bioactive isoflavone derived from soybeans, has shown prominent anti-tumor activity, whereas its exact molecular mechanism against CRC remains unclear. This study evaluated the anti-CRC effects of genistein using in vitro cell experiments and a nude mouse xenograft model, focusing on the LINC00355/miR-150/SGK1 axis and its downstream EGFR/PI3K/AKT and MAPK signaling pathways to explore the underlying regulatory mechanism. The results revealed that genistein dose-dependently inhibited CRC cell proliferation without obvious cytotoxicity to normal colon cells. It also induced cell cycle arrest and cancer cell apoptosis, and suppressed tumor migration and invasion. Mechanistically, genistein inhibited the activation of downstream oncogenic pathways by regulating the expression of the target molecular axis. In vivo assays further confirmed that genistein effectively repressed tumor growth with good safety. This study provides reliable experimental evidence for the development of genistein as a potential adjuvant therapeutic agent for CRC treatment.