Beneaththecomplexityofeverycancerliescriticaleventsincludingderegulatedcellproliferation, andsuppressedapoptosisthatprovidesaplatformnecessarytosupportfurtherneoplasticprogression. Cell proliferation is essentially an increase in the number of cells as a result of cell growth and cell division [29]. In our study, we evaluated the anti-proliferative effects of JPE using the MTT assay. There was a dose dependent suppression of cell proliferation in HCT-116 cells by JPE. At 30 µg/mL and 40 µg/mL (Figure 2A), there was suppression of proliferation (p < 0.05) by over 60% compared to control. Proliferation was also assessed by cell counting using an automated cell counter (Nexcelom) by treating the cells with JPE at 30 µg/mL and 40 µg/mL to confirm our observations with the MTT assay. Both concentrations resulted in more than 50% reduction in viable cell number (p < 0.05, Figure 2B). The suppression of proliferation by JPE in HCT-116 can be attributed to the presence of the identified compounds—-anthocyanins, flavonols and stilbenoids, which have been previously shown to suppress proliferation in colon cancer cells individually and in combination, in in vitro, in vivo, and in human studies [12,30,31]. Previous studies with anthocyanin rich chokeberry extracts have shown that suppression of proliferation in HT-29 colon cancer cells occurs via cell cycle arrest [32]. Thus, further mechanistic studies are required to study molecular mechanism of anti-proliferative action of JPE against colon cancer cells, including its effect on proliferative pathways and the cell cycle.
Beneaththecomplexityofeverycancerliescriticaleventsincludingderegulatedcellproliferation, andsuppressedapoptosisthatprovidesaplatformnecessarytosupportfurtherneoplasticprogression. Cell proliferation is essentially an increase in the number of cells as a result of cell growth and cell division [29]. In our study, we evaluated the anti-proliferative effects of JPE using the MTT assay. There was a dose dependent suppression of cell proliferation in HCT-116 cells by JPE. At 30 µg/mL and 40 µg/mL (Figure 2A), there was suppression of proliferation (p < 0.05) by over 60% compared to control. Proliferation was also assessed by cell counting using an automated cell counter (Nexcelom) by treating the cells with JPE at 30 µg/mL and 40 µg/mL to confirm our observations with the MTT assay. Both concentrations resulted in more than 50% reduction in viable cell number (p < 0.05, Figure 2B). The suppression of proliferation by JPE in HCT-116 can be attributed to the presence of the identified compounds—-anthocyanins, flavonols and stilbenoids, which have been previously shown to suppress proliferation in colon cancer cells individually and in combination, in in vitro, in vivo, and in human studies [12,30,31]. Previous studies with anthocyanin rich chokeberry extracts have shown that suppression of proliferation in HT-29 colon cancer cells occurs via cell cycle arrest [32]. Thus, further mechanistic studies are required to study molecular mechanism of anti-proliferative action of JPE against colon cancer cells, including its effect on proliferative pathways and the cell cycle.
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