Differential Induction of Cancer Cell Death by Root, Leaf, and Flower Extracts derived from Kalanchoe pinnata

Abstract

Kalanchoe pinnata is a perennial plant that grows wild in tropical regions and is traditionally used as a medicinal plant. Plants of the Kalanchoe genus have been shown to possess several effects, including antibacterial and antihypertensive properties. However, effects such as the induction of apoptosis in cancer cells have not been reported for any substance other than leaf extracts of this plant and remain unexplained. Therefore, in this study, we investigated the effects of extracts from various parts of K. pinnata (flowers, leaves, and roots) on human colon cancer cell death. We conducted the study using three colorectal cancer cell lines (HT-29, SW620, and DLD-1) and three types of extracts derived from the flowers, leaves, and roots of this plant. Each K. pinnata extract significantly reduced cell viability in a dose-dependent manner in all colon cancer cells. In particular, the root extract induced cancer cell death and inhibited proliferation at lower concentrations than the other extracts. For the colon cancer cells examined, caspase-dependent apoptosis was suggested as the primary mechanism, although cell death was observed in some cells without detectable caspase activation. K. pinnata extracts induced both apoptosis and necrosis in colorectal cancer cells. In addition, K. pinnata extracts increased protein level of cleaved caspase-9, caspase-3, and PARP in SW620 and DLD-1 cells. The decrease in mitochondrial membrane potential was confirmed for all extracts, however caspase-mediated apoptosis was not observed in all cell lines, indicating the need for further investigation. Taken together, our results indicate the potential of the plant K. pinnata and the bioactive compounds it contains as new candidates for adjuvant therapy in colorectal cancer. In the future, it will be necessary to examine the relationship with genetic mutations in each cell line and to investigate the details of the cell death mechanism.