Kaempferitrin inhibits colorectal cancer cells by inducing reactive oxygen species and modulating PI3K/AKT signalling pathway

Colorectal cancer is a life-threatening malignancy of high invasive death worldwide, despite improvements in conventional chemotherapy. Hence, there is an urgent need for new and effective anti-colorectal chemotherapeutic agents. Kaempferitrin can inhibit colon cancer cell viability, apoptotic induction, and reactive oxygen species (ROS) generation in a concentration-dependent way. Kaempferitrin had a cytotoxic and anti-proliferative effect on HT-29 colorectal cancer cells at a dosage of 30 mu M, regulate apoptotic cell death, cell proliferation, and the cellular antioxidant system. Hyperoxia, cellular stress, ROS, and oxidative damage are the regulators of cancer cells. Increased sensitivity towards oxidative stress is caused by a change in redox state caused by enhanced ROS generation. In HT-29 cells, kaempferitrin also activated caspase-3 and enhanced the ratios of cleaved PARP protein expression, triggering caspase-dependent death. These kaempferitrin-induced processes also correlate with PI3K/AKT, implying downstream targeting of the cancer cell pathway. These findings suggest that kaempferitrin could be a promising therapeutic agent for the treatment of CRC, since it inhibits CRC cell proliferation and induces apoptosis via the PI3K/AKT signalling pathway.

Automated summary

Kaempferitrin shows promise as a potential therapeutic agent for colorectal cancer, as it inhibits cancer cell proliferation and induces apoptosis through the PI3K/AKT signaling pathway.