Inorganic titanium dioxide nanoparticles induces cytotoxicity in colon cancer cells

Globally, colorectal cancer (CRC) is responsible for 10% of the commonly diagnosed cancers. Almost ten million colo-rectal cancer deaths occurred in 2020. Existing treatment strategies often led to several off-target and adverse effects. A variety of studies have shown the anti-cancer potential of titanium oxide nanoparticles (TiO2). Therefore, in this study, we have synthesized TiO2 using Lactobacillus and its cytotoxic potential has been evaluated in HT-29 cells, a human CRC cell line. The morphology of TiO2 nanoparticles was analyzed by scanning electron microscope. The cytotoxicity was investigated by MTT assay. Apoptosis-related morphology was analyzed by acridine orange/ethidium bromide staining. Mitochondrial health was analyzed by rhodamine staining. Caspase 3 was analyzed by immunofluorescence. Lactobacillus mediated TiO2 treatments induced cytotoxicity in HT-29 cells. These nanoparticles also induced intracellular reactive oxygen species (ROS) generation and caused apoptosis-related morphological changes in colon cancer cells. TiO2 treatments decreased bcl2 and increased bax, apaf-1, caspase-9 and -3 gene expressions and this treatment also caused mitochondrial dissipation and cytochrome c release. The current study results suggest that TiO2 is capable of inducing cytotoxicity in colon cancer cells by intracellular ROS accumulation. The ROS induction was associated with mitochondrial toxicity and cytochrome c increase can be related to the induction of intrinsic apoptosis. These results indicate that TiO2 could cause apoptosis by activating intrinsic apoptotic pathway and generating ROS in HT-29 cells. These results suggest that TiO2 can be used as a lung cancer therapeutic agent after necessary in vivo and clinical studies.

Automated summary

TiO2 synthesized with Lactobacillus shows cytotoxicity in colon cancer cells by inducing apoptosis and generating intracellular reactive oxygen species (ROS). Moreover, TiO2 causes mitochondrial damage and cytochrome c release, leading to apoptosis by activating the intrinsic apoptotic pathway.