Colon caspase 14 expression

Swamy et al. ° used human HT-29 colon cancer cells to study the effectiveness of lovastatin and celecoxib, individually or in combination on the induction of apoptosis in human HT-29 colon cancer cells. They also studied the modulatory effect of lovastatin and celecoxib on lamin B levels, caspase-3 activity and expression in relationship to apoptosis in colon cancer cell lines. Importantly, their results showed that agents with different modes of action, when utilized in combinations, will induce apoptosis synergistically by enhancing caspase-3 activities. These authors concluded that the regulation of apoptosis is enhanced by selective agents such as lovastatin and celecoxib combinations for colon cancer prevention. 

Suppressing mechanism This mechanism includes elimination of tumor cells, including growth inhibition by induction of cell-cycle arrest or apoptosis. Apigenin has been shown to induce G2/M arrest in SW480 and Caco-2 human colon carcinoma cells [40], Resveratrol and quercetin are reported to induce the expression of caspase-3 promoting apoptosis, arresting cells in G1 phase of the cell cycle, and decrease tiunor cell invasion [41]. 

Apple juice phenolic compound extracts have the property to induce apoptosis in HT-29 cells [147]. Quercetin and phloretin dose-dependently induced both caspase-3 activity and DNA cleavage under serum-free conditions. Phloretin at 100 pM induced both the death receptor as well as the mitochondrial pathway of apoptosis induction, detected by activation of the initiator caspases-8 and -9 and the effector caspases-3 and -7 as well as by PARP cleavage. Activation of caspase-9 was accompanied by release of cytochrome c and the mitochondrial protein Smac/DIABLO from the mitochondria to the cytoplasm, and upregulation of proapoptotic Bax levels [43,44,148]. In general, berry extracts have the ability to stimulate apoptosis of the HT-29, COX-2-expressing colon cancer cells. Black raspberry and strawberry extracts showed the most significant proapoptotic effects against this cell line [43] (Tables 1 and 6). 

Su and coworkers investigated the induction of apoptosis by Tan-I at 1-10 pg/mL in human colon cancer Colo 205 cells. Tan-I reduced cell growth in a concentration-dependent manner, inducing apoptosis accompanied by an increase in TUNEL-stained cells in the sub-Gl fraction. The treatment with Tan-I at 0, 1, 2.5, 5, and 10 pg/mL for 72 h increased the percentage of cells in sub-Gl phase from 3.83% to 7.22%, 8.68%, 14.4%, and 32.98%, respectively. The expression of p53, p21, bax, and caspase-3 increased in Tan-I-treated cells. The authors suggested that Tan-I induces apoptosis in Colo 205 cells through both mitochondrial-mediated intrinsic ceU-death pathways and p21-mediated GO/Gl cell cycle arrest [50]. 

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