Abstract
ABSTRACTThe pro-apoptotic and inhibitory effects of the aflavin-3,3′-digallate (TFDG), which is the typical pigment in black tea, have been demonstrated in many cancer cell lines. However, TFDG is not stable in general culture conditions. So, to what extent TFDG or which degradation products of TFDG play an antitumor role is still unclear. In this study, we evaluated the effect of different treatments of TFDG on HCT116 cells. Compared with the control, both TFDG and O-TFDG (the TFDG that was pre-incubated in an incubator at 37°C for 3 hbefore adding into 96-well plates) significantly inhibited HCT116 cell growth. However, pre-treated TFDG was far better than TFDG. The IC50 values of TFDG and O-TFDG-3 were 17.26 μM and 8.98 μM, respectively (the cells were treated by O-TFDG for only 3 h, after which the media were replaced by fresh media for another 69 h incubation). Cell-cycle analysis revealed that 20 μM of O-TFDG and O-TFDG-3 caused cell-cycle arrest at G2 phase in HCT116 cells. Western blot analysis also demonstrated that the anti-inflammatory effect of O-TFDG-3 is stronger than that of TFDG by decreasing COX-2 and iNOS. On the other hand, O-TFDG induced HCT116 cells apoptosis mainly by increasing the expression of p53, p21, and cleaved caspase-3. The current study demonstrated that O-TFDG had a higher inhibitory effect on HCT116 cells than TFDG, and sowe may inferfromthis that the degradation products of TFDG play a key role against tumors.
Highlights
The pro-apoptotic and inhibitory effects of the aflavin-3,3′-digallate (TFDG), which is the typical pigment in black tea, have been demonstrated in many cancer cell lines
Numerous investigations have indicated that TFDG is a remarkable chemopreventive and chemotherapeutic agent against various cell lines [22,23]
We investigated the effect of different treatments of TFDG on the HCT116 cell line
Summary
The pro-apoptotic and inhibitory effects of the aflavin-3,3′-digallate (TFDG), which is the typical pigment in black tea, have been demonstrated in many cancer cell lines. The current study demonstrated that O-TFDG had a higher inhibitory effect on HCT116 cells than TFDG, and sowe may inferfromthis that the degradation products of TFDG play a key role against tumors. TFDG might promote degradation of the Raf-1-hsp complex These mechanisms lead to a decrease in phospho-MEK1. Theaflavins decrease antioxidant MnSOD and increase pro-oxidant proline oxidase in Wt-p53 MCF-7 cells, but the same change has not been observed in mutant p53-containing MDAMB-231 cells and p53-knock-out MCF-7 cells This clearly suggests that theaflavins maintain the balance between proand antioxidant enzymes in a p53-dependent manner to generate ROS in MCF-7 cells [10]. We studied the effect of different treatments of TFDG on HCT116 cell line
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