Luteoloside induces apoptosis in human HCT116 colorectal cancer cells via mitochondrial and PI3K/AKT signaling pathways

Luteoloside (LUS), a flavonoid isolated from the flower stem leaves of honeysuckle, exhibits anticancer activity. Nevertheless, further comprehensive and articulate research is still needed to determine the precise anticolorectal cancer (CRC) effects of LUS, as well as its possible molecular mechanism and biological target. Using the colorectal cancer cell line HCT116, we examined the anti-cancer characteristics and underlying mechanisms of LUS. Our results demonstrate that LUS efficiently inhibited HCT116 cell proliferation, resulting in significant changes to cell shape. Furthermore, LUS treatment resulted in cell cycle arrest, specifically targeting the G2/M phase, accompanied by apoptosis of colorectal cancer cells, which was dependent on the inhibition of the PI3K/AKT/mTOR pathway and intracellular reactive oxygen species (ROS) generation. Through damage to the mitochondrial membrane, LUS may induce colorectal cancer cells to undergo apoptosis; lower the potential of the mitochondrial membrane and increase the level of reactive oxygen species; increase the release of cytochrome c, which lowers Delta psi m; upregulate the expression of Bax, cytochrome c, and p21; and lower the levels of Bcl-xl, Bcl-2, caspase-3, and caspase-9. LUS holds the potential as dietary ingredient in the treatment of CRC, which can be used in the development of personalized nutrition.