Despite the recent advances in diagnostic and surgical techniques, colorectal cancer (CRC) remains the third most frequently diagnosed cancer and second most common cause of cancer-related mortality worldwide (Li, 2018). CRC is mainly treated by surgical removal, radiotherapy, chemotherapy, or a combination of surgery and chemotherapy (Yang et al., 2017). Despite various treatment strategies, many patients with CRC continue to experience relapse-hence, improved chemotherapeutic agents that can effectively induce apoptosis in CRC cells are urgently needed.Apoptosis involves two types of signaling pathways. The extrinsic pathway is initiated by the binding of specific receptors on the cell surface, called death receptors, with an extracellular ligand. This involves the binding of Fas receptors, known as differentiation clusters, to Fas ligands, and tumor necrosis factor (TNF) receptors to TNF (Ashkenazi, 2008;Fulda, 2015). These binding events induce the activation of caspase 8 in the intracellular domain of the receptor (O'Brien and Kirby, 2008;Wong, 2011). Activated caspase 8 can affect mitochondria or further activate caspase 3 (Ashkenazi, 2008). The intrinsic pathway is initiated by the loss of mitochondrial membrane potential, resulting in the release of internalized cytochrome c into the cytoplasm (Saelens et al., 2004). The released cytochrome c activates caspase 3 by forming a complex called the apoptosome with apoptosis protease activator 1 and caspase 9 (Elmore, 2007). A family of proteins called B-cell lymphoma