scholarly journals Cyclooxygenase-2 and 5-lipoxygenase pathways in diosgenin-induced apoptosis in HT-29 and HCT-116 colon cancer cells

2010 ◽  
Vol 36 (5) ◽  
Author(s):  
Liagre
2010 ◽  
Author(s):  
Lloyd F. Alfonso ◽  
Raghavender Chivukula ◽  
Srinivasan Marimuthu ◽  
Jayarama B. Gunaje

2008 ◽  
Vol 32 (10) ◽  
pp. 1207-1214 ◽  
Author(s):  
J PARK ◽  
J CHANG ◽  
K BAE ◽  
K LEE ◽  
S CHOI ◽  
...  

2016 ◽  
Vol 14 (5) ◽  
pp. 4559-4566 ◽  
Author(s):  
Lin Yang ◽  
Yanqing Liu ◽  
Mei Wang ◽  
Yayun Qian ◽  
Xiaoyun Dong ◽  
...  

2009 ◽  
Vol 296 (5) ◽  
pp. G1060-G1068 ◽  
Author(s):  
Do Y. Lim ◽  
Jung Han Yoon Park

Fisetin, or 3,3′,4′,7-tetrahydroxyflavone, is present in fruits and vegetables and has been previously reported to inhibit the proliferation of a variety of cancer cells (Lu X, Jung J, Cho HJ, Lim do Y, Lee HS, Chun HS, Kwon DY, Park JH. J Nutr 135: 2884–2890, 2005). We have demonstrated in a previous work that 20–60 μmol/l fisetin inhibits cyclin-dependent kinase activities resulting in cell cycle arrest in HT-29 colon cancer cells. In the present study, we attempted to characterize the mechanisms by which fisetin induces apoptosis in HCT-116 cells. DNA condensations, cleavage of poly(ADP-ribose) polymerase (PARP), and cleavage of caspases 9, 7, and 3 were induced in HCT-116 cells treated with 5–20 μmol/l of fisetin. Fisetin induced a reduction in the protein levels of antiapoptotic Bcl-xL and Bcl-2 and an increase in the levels of proapoptotic Bak and Bim. Fisetin did not affect the Bax protein levels, but induced the mitochondrial translocation of this protein. Fisetin also enhanced the permeability of the mitochondrial membrane and induced the release of cytochrome c and Smac/Diablo. Additionally, fisetin caused an increase in the protein levels of cleaved caspase-8, Fas ligand, death receptor 5, and TNF-related apoptosis-inducing ligand, and the caspase-8 inhibitor Z-IETD-FMK suppressed fisetin-induced apoptosis and the activation of caspase-3. Furthermore, fisetin increases p53 protein levels, and the inhibition of p53 expression by small interference RNA resulted in a decrease in the fisetin-induced translocation of Bax to the mitochondria, release of mono- and oligonucleosome in the cytoplasm, and PARP cleavage. These results show that fisetin induces apoptosis in HCT-116 cells via the activation of the death receptor- and mitochondrial-dependent pathway and subsequent activation of the caspase cascade. The induction of p53 results in the translocation of Bax to the mitochondria, which contributes to fisetin-induced apoptosis in HCT-116 cells.


2007 ◽  
Vol 1095 (1) ◽  
pp. 496-503 ◽  
Author(s):  
Y. M. KIM ◽  
J.-T. HWANG ◽  
D. W. KWAK ◽  
Y. K. LEE ◽  
O. J. PARK

2017 ◽  
Vol 64 (2) ◽  
Author(s):  
Tomasz Przybyła ◽  
Monika Sakowicz-Burkiewicz ◽  
Izabela Maciejewska ◽  
Hanna Bielarczyk ◽  
Tadeusz Pawełczyk

Adjuvant chemotherapy with 5-fluorouracil remains the basic treatment for patients with advanced colorectal carcinoma. The major obstacle in successful treatment is an ability of CRC cells to acquire chemoresistance. Here we examined the impact of ID1 silencing on the sensitivity of CRC cells to 5-FU. To suppress ID1 expression in HT-29 and HCT-116 cells the cells were transduced with a lentiviral vector carrying the ID1 silencing sequence. Cells with silenced ID1 showed altered expression of epithelial and mesenchymal markers and exhibited increased proliferation rate compared to the parental cells. HCT-116 cells with suppressed ID1 became sensitized to 5-FU and this was not observed in HT-29 cells. Silencing ID1 resulted in altered expression of genes encoding enzymes metabolizing 5-FU. HT-29 cells with suppressed ID1 had significantly reduced mRNA level for thymidine phosphorylase, uridine-cytydine kinase 2 and dihydropyrimidine dehydrogenase. ID1 suppression in HCT-116 cells resulted in an increase of mRNA level for thymidine phosphorylase, thymidyne kinase and uridine-cytydine kinase 2 with concurrent drop of dihydropyrimidine dehydrogenase and thymidylate synthetase mRNA levels. In conclusion ID1 expression impacts the sensitivity of colon cancer cells to 5-FU and may be considered as potential predictive marker in CRC treatment.


2014 ◽  
Vol 156 ◽  
pp. 277-289 ◽  
Author(s):  
Soheil Zorofchian Moghadamtousi ◽  
Hamed Karimian ◽  
Elham Rouhollahi ◽  
Mohammadjavad Paydar ◽  
Mehran Fadaeinasab ◽  
...  

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