Quinacrine causes apoptosis in human cancer cell lines through caspase-mediated pathway and regulation of small-GTPase.

Quinacrine (QC), an FDA-approved anti-malarial drug, has shown to have anticancer activities. Due to its 'shotgun' nature, QC has become an inevitable candidate for combination chemotherapy. There is lack of study of the molecular interplay between colorectal cancer (CRC) microenvironment and its metastasis. In this study, we focused on the differential anti-cancerous effect of QC on two different human cancer cell lines, HCT 116 and INT 407. Results suggest that cytotoxicity increased in both the cell lines with an increase in QC concentration. The expression patterns of small-GTPases and caspases were altered significantly in QC-treated cells compared to non-treated cells. HSP70 and p53 showed comparable differences in the expression pattern. The wound-healing assay showed an increase in the denuded zone, with an increase in the concentration of QC. The formation of apoptotic nuclei increased with a rise in the concentration of QC in both the cell lines. The decrease and increase in caspase 9 and caspase 3 expression respectively were studied, confirming apoptosis by the extrinsic pathway.