scholarly journals Caspase-3 regulates the migration, invasion and metastasis of colon cancer cells

2018 ◽  
Vol 143 (4) ◽  
pp. 921-930 ◽  
Author(s):  
Min Zhou ◽  
Xinjian Liu ◽  
Zonghai Li ◽  
Qian Huang ◽  
Fang Li ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Colon Cancer Cells ◽  
Invasion And Metastasis

scholarly journals Integrated analysis of potential pathways by which aloe-emodin induces the apoptosis of colon cancer cells

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Dongxiao Jiang ◽  
Shufei Ding ◽  
Zhujun Mao ◽  
Liyan You ◽  
Yeping Ruan
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Time Dependent ◽  
Integrated Analysis ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Dapi Staining ◽  
Aloe Emodin

Abstract Background Colon cancer is a malignant gastrointestinal tumour with high incidence, mortality and metastasis rates worldwide. Aloe-emodin is a monomer compound derived from hydroxyanthraquinone. Aloe-emodin produces a wide range of antitumour effects and is produced by rhubarb, aloe and other herbs. However, the mechanism by which aloe-emodin influences colon cancer is still unclear. We hope these findings will lead to the development of a new therapeutic strategy for the treatment of colon cancer in the clinic. Methods We identified the overlapping targets of aloe-emodin and colon cancer and performed protein–protein interaction (PPI), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. In addition, we selected apoptosis pathways for experimental verification with cell viability, cell proliferation, caspase-3 activity, DAPI staining, cell cycle and western blotting analyses to evaluate the apoptotic effect of aloe-emodin on colon cancer cells. Results The MTT assay and cell colony formation assay showed that aloe-emodin inhibited cell proliferation. DAPI staining confirmed that aloe-emodin induced apoptosis. Aloe-emodin upregulated the protein level of Bax and decreased the expression of Bcl-2, which activates caspase-3 and caspase-9. Furthermore, the protein expression level of cytochrome C increased in a time-dependent manner in the cytoplasm but decreased in a time-dependent manner in the mitochondria. Conclusion These results indicate that aloe-emodin may induce the apoptosis of human colon cancer cells through mitochondria-related pathways.

scholarly journals Antiproliferative and apoptosis-inducing effects of maslinic and oleanolic acids, two pentacyclic triterpenes from olives, on HT-29 colon cancer cells

2008 ◽  
Vol 100 (1) ◽  
pp. 36-43 ◽  
Author(s):  
M. Emília Juan ◽  
Joana M. Planas ◽  
Valentina Ruiz-Gutierrez ◽  
Hannelore Daniel ◽  
Uwe Wenzel
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Oleanolic Acid ◽  
Caspase 3 ◽  
Hydroxyl Group ◽  
Colon Cancer Cells ◽  
Maslinic Acid ◽  
Olive Fruit ◽  
Pentacyclic Triterpenes ◽  
Ht 29

We have previously reported the anticarcinogenic effects of an olive fruit extract composed of pentacyclic triterpenes, the main components of which are maslinic acid (73·25 %) and oleanolic acid (25·75 %). Here we examined the effects of the individual components on proliferation, necrosis and apoptosis rates by fluorescence-based techniques in human HT-29 colon cancer cells. Oleanolic acid showed moderate antiproliferative activity, with an ec50 of 160·6 (se 10·6) μmol/l, and moderate cytotoxicity at high concentrations ( ≥ 250 μmol/l). On the other hand, maslinic acid inhibited cell growth with an ec50 of 101·2 (se 7·8) μmol/l, without necrotic effects. Oleanolic acid, which lacks a hydroxyl group at the carbon 2 position, failed to activate caspase-3 as a prime apoptosis protease. In contrast, maslinic acid increased caspase-3-like activity at 10, 25 and 50 μmol/l by 3-, 3·5- and 5-fold over control cells, respectively. The detection of ROS in the mitochondria, which serve as pro-apoptotic signal, evidenced the different bioactivity of the two triterpenes. Confocal microscopy analysis revealed that maslinic acid generated superoxide anions while oleanolic acid-treated cells did not differ from the control. Completion of apoptosis by maslinic acid was confirmed microscopically by the increase in plasma membrane permeability, and detection of DNA fragmentation. In conclusion, the anticancer activity observed for olive fruit extracts seems to originate from maslinic acid but not from oleanolic acid. Maslinic acid therefore is a promising new compound for the chemoprevention of colon cancers.

scholarly journals Autocrine induction of invasion and metastasis by tumor-associated trypsin inhibitor in human colon cancer cells

Oncogene ◽  
2008 ◽  
Vol 27 (29) ◽  
pp. 4024-4033 ◽  
Author(s):  
V Gouyer ◽  
D Fontaine ◽  
P Dumont ◽  
O de Wever ◽  
H Fontayne-Devaud ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Trypsin Inhibitor ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Invasion And Metastasis ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells

scholarly journals Ceramide synthase 6 modulates TRAIL sensitivity and nuclear translocation of active caspase-3 in colon cancer cells

Oncogene ◽  
2009 ◽  
Vol 28 (8) ◽  
pp. 1132-1141 ◽  
Author(s):  
S White-Gilbertson ◽  
T Mullen ◽  
C Senkal ◽  
P Lu ◽  
B Ogretmen ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Nuclear Translocation ◽  
Ceramide Synthase ◽  
Colon Cancer Cells ◽  
Trail Sensitivity ◽  
Active Caspase

Effect of polyamide nanoparticles on apoptosis of colon cancer cells induced by survivin antisense oligonucleotide

2020 ◽  
Vol 10 (9) ◽  
pp. 1573-1580
Author(s):  
Yongqiang Xu ◽  
Weibiao Ye ◽  
Chan Zhou ◽  
Yuling Li ◽  
Jianfang He
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Significant Difference ◽  
Microfilament System ◽  
Human Colon Cancer Cells

In this study, we aimed to observe the effect of polyamidoamine (PAMAM) liposomes on the apoptosis of human colon cancer cells induced by survivin antisense oligonucleotides (ASODNs). PAMAM liposomes and PAMAM were mixed with survivin ASODNs to obtain antisense gene transfection complexes. In addition, the zeta potentials and encapsulation rates of the complexes were measured. The two gene-containing complexes were transfected into HT-29 colon cancer cells to observe changes in cell morphology, detect the inhibitory effect on tumor cells and changes in apoptosis, and observe changes in the cytoskeleton microfilament system using laser confocal microscopy. Caspase-3 activity in the cells was determined using a kinase activity assay, and p38 mitogen-activated protein kinase (p38 MAPK) activity in the cells was measured using immunoprecipitation analysis. The results showed that the zeta potential of the PAMAM liposome-survivin-ASODN complex was higher than that of the PAMAM-survivin-ASODN complex (P < 0.05). There was no significant difference in the gene encapsulation rates between the two complexes (P > 0.05). PAMAM liposomes may efficiently deliver survivin ASODNs to human colon cancer cells, reduce the expression of survivin protein and at the same time induce G2/M phase arrest in cells, and activate caspase-3 by activating p38 MAPK. Cleavage of caspase-3 destroys the structure of the intracellular skeletal microfilament system, finally resulting in apoptosis of colon cancer cells.

Ginsenoside Rg3 Suppresses Epithelial-Mesenchymal Transition via Downregulating Notch-Hes1 Signaling in Colon Cancer Cells

2020 ◽  
pp. 1-19
Author(s):  
Xiao Li ◽  
Wei Liu ◽  
Chong Geng ◽  
Tingting Li ◽  
Yanni Li ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Ginsenoside Rg3 ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
E Cadherin

Invasion and metastasis are the major causes leading to the high mortality of colon cancer. Ginsenoside Rg3 (Rg3), as a bioactive ginseng compound, is suggested to possess antimetastasis effects in colon cancer. However, the underlying molecular mechanisms remain unclear. In this study, we reported that Rg3 could effectively inhibit colon cancer cell invasion and metastasis through in vivo and in vitro studies. In addition, Rg3 suppressed the epithelial–mesenchymal transition (EMT) of HCT15 cells and SW48 cells evidenced by detecting EMT related markers E-cadherin, vimentin, and snail expression. Furthermore, inhibition of Notch signaling by LY411,575 or specific Hes1 siRNA obviously repressed colon cancer cell migration and metastasis, and induced increase in E-cadherin and decrease in vimentin and snail. Meanwhile, the expression of NICD and Hes1 was obviously decreased in the presence of Rg3. However, Rg3 failed to suppress EMT in Hes1 overexpressed colon cancer cells. In particular, Rg3 significantly reversed IL-6-induced EMT promotion and blocked IL-6- induced NICD and Hes1 upregulations. Overall, these findings suggested that Rg3 could inhibit colon cancer migration and metastasis via suppressing Notch-Hes1-EMT signaling.

scholarly journals Cleavage of GSDME by caspase-3 determines lobaplatin-induced pyroptosis in colon cancer cells

2019 ◽  
Vol 10 (3) ◽  
Author(s):  
Junhui Yu ◽  
Shan Li ◽  
Jie Qi ◽  
Zilu Chen ◽  
Yunhua Wu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Colon Cancer Cells

scholarly journals HSP90 Inhibitors, Geldanamycin and Radicicol, Enhance Fisetin-Induced Cytotoxicity via Induction of Apoptosis in Human Colonic Cancer Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Ming-Shun Wu ◽  
Gi-Shih Lien ◽  
Shing-Chuan Shen ◽  
Liang-Yo Yang ◽  
Yen-Chou Chen
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Caspase 3 ◽  
P53 Protein ◽  
Colon Cancer Cells ◽  
Hsp90 Inhibitors ◽  
Dna Ladder ◽  
Human Colon Cancer ◽  
Bax Protein

We revealed the cytotoxic effect of the flavonoid, fisetin (FIS), on human COLO205 colon cancer cells in the presence and absence of the HSP90 inhibitors, geldanamycin (GA) and radicicol (RAD). Compared to FIS treatment alone of COLO205 cells, GA and RAD significantly enhanced FIS-induced cytotoxicity, increased expression of cleaved caspase-3 and the PAPR protein, and produced a greater density of DNA ladder formation. GA and RAD also reduced the MMPs with induction of caspase-9 protein cleavage in FIS-treated COLO205 cells. Increased caspase-3 and -9 activities were detected in COLO205 cells treated with FIS+GA or FIS+RAD, and the intensity of DNA ladder formation induced by FIS+GA was reduced by adding the caspase-3 inhibitor, DEVD-FMK. A decrease in Bcl-2 but not Bcl-XL or Bax protein by FIS+GA or FIS+RAD was identified in COLO205 cells by Western blotting. A reduction in p53 protein with increased ubiquitin-tagged proteins was observed in COLO205 cells treated with FIS+GA or FIS+RAD. Furthermore, GA and RAD reduced the stability of the p53 protein in COLO205 cells under FIS stimulation. The evidence supports HSP90 inhibitors possibly sensitizing human colon cancer cells to FIS-induced apoptosis, and treating colon cancer by combining HSP90 inhibitors with FIS deserves further in vivo study.

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