scholarly journals Casticin, a flavonoid, potentiates TRAIL-induced apoptosis through modulation of anti-apoptotic proteins and death receptor 5 in colon cancer cells

2012 ◽  
Vol 29 (2) ◽  
pp. 474-480 ◽  
Author(s):  
SAN-YUAN TANG ◽  
MEI-ZUO ZHONG ◽  
GUANG-JIN YUAN ◽  
SU-PING HOU ◽  
LEI-LAN YIN ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Death Receptor 5 ◽  
Colon Cancer Cells ◽  
Apoptotic Proteins ◽  
Induced Apoptosis

scholarly journals 2-Methoxy-5-Amino-N-Hydroxybenzamide Sensitizes Colon Cancer Cells to TRAIL-Induced Apoptosis by Regulating Death Receptor 5 and Survivin Expression

2011 ◽  
Vol 10 (10) ◽  
pp. 1969-1981 ◽  
Author(s):  
Carmine Stolfi ◽  
Roberta Caruso ◽  
Eleonora Franzè ◽  
Angelamaria Rizzo ◽  
Angela Rotondi ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Survivin Expression ◽  
Death Receptor 5 ◽  
Colon Cancer Cells ◽  
Induced Apoptosis

Diosgenin induces death receptor-5 through activation of p38 pathway and promotes TRAIL-induced apoptosis in colon cancer cells

2011 ◽  
Vol 301 (2) ◽  
pp. 193-202 ◽  
Author(s):  
C. Lepage ◽  
D.Y. Léger ◽  
J. Bertrand ◽  
F. Martin ◽  
J.L. Beneytout ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Death Receptor 5 ◽  
Colon Cancer Cells ◽  
Induced Apoptosis ◽  
P38 Pathway

scholarly journals Myeloid zinc finger 1 mediates sulindac sulfide-induced upregulation of death receptor 5 of human colon cancer cells

2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Mano Horinaka ◽  
Tatsushi Yoshida ◽  
Mitsuhiro Tomosugi ◽  
Shusuke Yasuda ◽  
Yoshihiro Sowa ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Human Colon ◽  
Death Receptor 5 ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Sulindac Sulfide ◽  
Myeloid Zinc Finger ◽  
Human Colon Cancer Cells

scholarly journals Artemisinin Derivatives Stimulate DR5-Specific TRAIL-Induced Apoptosis by Regulating Wildtype P53

Cancers ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 2514
Author(s):  
Xinyu Zhou ◽  
Sietske N. Zijlstra ◽  
Abel Soto-Gamez ◽  
Rita Setroikromo ◽  
Wim J. Quax
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Dependent Manner ◽  
Death Receptor 5 ◽  
Novel Therapy ◽  
Artemisinin Derivatives ◽  
The Status ◽  
Cervical Cancer Cells ◽  
Induced Apoptosis

Artemisinin derivatives, widely known as commercial anti-malaria drugs, may also have huge potential in treating cancer cells. It has been reported that artemisinin derivatives can overcome resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis in liver and cervical cancer cells. In our study, we demonstrated that artesunate (ATS) and dihydroartemisinin (DHA) are more efficient in killing colon cancer cells compared to artemisinin (ART). ATS/DHA induces the expression of DR5 in a P53 dependent manner in HCT116 and DLD-1 cells. Both ATS and DHA overcome the resistance to DHER-induced apoptosis in HCT116, mainly through upregulating death receptor 5 (DR5). We also demonstrate that DHA sensitizes HCT116 cells to DHER-induced apoptosis via P53 regulated DR5 expression in P53 knockdown assays. Nevertheless, a lower effect was observed in DLD-1 cells, which has a single Ser241Phe mutation in the P53 DNA binding domain. Thus, the status of P53 could be one of the determinants of TRAIL resistance in some cancer cells. Finally, the combination treatment of DHA and the TRAIL variant DHER increases cell death in 3D colon cancer spheroid models, which shows its potential as a novel therapy.

scholarly journals Gossypol Induces Death Receptor-5 through Activation of the ROS-ERK-CHOP Pathway and Sensitizes Colon Cancer Cells to TRAIL

2010 ◽  
Vol 285 (46) ◽  
pp. 35418-35427 ◽  
Author(s):  
Bokyung Sung ◽  
Jayaraj Ravindran ◽  
Sahdeo Prasad ◽  
Manoj K. Pandey ◽  
Bharat B. Aggarwal
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Death Receptor 5 ◽  
Colon Cancer Cells

scholarly journals Death receptor 5 is activated by fucosylation in colon cancer cells

FEBS Journal ◽  
2019 ◽  
Vol 286 (3) ◽  
pp. 555-571 ◽  
Author(s):  
Baojie Zhang ◽  
Ingrid A. M. Roosmalen ◽  
Carlos R. Reis ◽  
Rita Setroikromo ◽  
Wim J. Quax
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Death Receptor 5 ◽  
Colon Cancer Cells

Induction of p53 contributes to apoptosis of HCT-116 human colon cancer cells induced by the dietary compound fisetin

2009 ◽  
Vol 296 (5) ◽  
pp. G1060-G1068 ◽  
Author(s):  
Do Y. Lim ◽  
Jung Han Yoon Park
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Parp Cleavage ◽  
Caspase 8 ◽  
Colon Cancer Cells ◽  
Protein Levels ◽  
Hct 116 ◽  
Hct 116 Cells ◽  
Induced Apoptosis

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.

scholarly journals Epigallocatechin-3-Gallate Induces Apoptosis as a TRAIL Sensitizer via Activation of Caspase 8 and Death Receptor 5 in Human Colon Cancer Cells

Biomedicines ◽  
2020 ◽  
Vol 8 (4) ◽  
pp. 84 ◽  
Author(s):  
Oh Sung Kwon ◽  
Ji Hoon Jung ◽  
Eun Ah Shin ◽  
Ji Eon Park ◽  
Woon Yi Park ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Caspase 8 ◽  
Mrna Levels ◽  
Death Receptor 5 ◽  
Colon Cancer Cells ◽  
Antitumor Effects ◽  
Hct116 Cells

Though epigallocatechin-3-gallate (EGCG), a major compound of green tea, has anti-diabetes, anti-obesity, anti-inflammatory, and antitumor effects, the underlying antitumor molecular mechanism of EGCG was not fully understood so far. Here the sensitizing effect of EGCG to tumor-necrosis-factor-related apoptosis-inducing ligand (TRAIL) was examined in colorectal cancers. Cotreatment of EGCG and TRAIL synergistically enhanced cytotoxicity and sub G1 accumulation, increased the number of terminal deoxynucleotidyl transferase-dT-mediated dUTP nick end labelling (TUNEL)-positive cells in SW480 and HCT116 cells. Furthermore, this cotreatment promoted the cleavages of poly (adenosine diphosphate-ribose) polymerase (PARP) and induced caspase 8 activation compared to TRAIL or EGCG alone in SW480 and HCT116 cells. Of note, cotreatment of EGCG and TRAIL increased the expression of death receptor 5 (DR5) at protein and mRNA levels and also DR5 cell surface level in colon cancer cells. Conversely, depletion of DR5 reduced the apoptotic activity of cotreatment of EGCG and TRAIL to increase cytotoxicity, sub-G1 population and PARP cleavages in colon cancer cells. Overall, our findings provide evidence that EGCG can be a sensitizer of TRAIL via DR5 and caspase 8 mediated apoptosis in colorectal cancer cells.

scholarly journals Gossypol induces death receptor-5 through activation of ROS-ERK-CHOP pathway and sensitizes colon cancer cells to TRAIL.

2016 ◽  
Vol 291 (32) ◽  
pp. 16923-16923 ◽  
Author(s):  
Bokyung Sung ◽  
Jayaraj Ravindran ◽  
Sahdeo Prasad ◽  
Manoj K. Pandey ◽  
Bharat B. Aggarwal
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Death Receptor ◽  
Death Receptor 5 ◽  
Colon Cancer Cells
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