369. TLR-4 Signalling Potentiates Colon Cancer Cell Adhesion Via Nox-derived Reactive Oxygen Species

2012 ◽  
Vol 38 (9) ◽  
pp. 843
Author(s):  
P. O'Leary ◽  
J.H. Wang ◽  
T.G. Cotter ◽  
H.P. Redmond
Keyword(s):  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Cell Adhesion ◽  
Cancer Cell ◽  
Reactive Oxygen ◽  
Colon Cancer Cell ◽  
Oxygen Species ◽  
Cancer Cell Adhesion

Tu1829 The Effects of Ursodeoxycholic Acid on Cell Cycle, Reactive Oxygen Species, and Proliferation of Colon Cancer Cell

2016 ◽  
Vol 150 (4) ◽  
pp. S955
Author(s):  
Su Young Kim ◽  
Eun-Kyoung Kim ◽  
A Reum Jeong ◽  
Yoon Jae Kim ◽  
Eui Joo Kim ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Cycle ◽  
Colon Cancer ◽  
Ursodeoxycholic Acid ◽  
Cancer Cell ◽  
Reactive Oxygen ◽  
Colon Cancer Cell ◽  
Oxygen Species

scholarly journals CXCL2-CXCR2 axis mediates αV integrin-dependent peritoneal metastasis of colon cancer cells

2021 ◽  
Author(s):  
Mattias Lepsenyi ◽  
Nader Algethami ◽  
Amr A. Al-Haidari ◽  
Anwar Algaber ◽  
Ingvar Syk ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Colon Cancer Cells ◽  
Cancer Cell Adhesion ◽  
And Migration ◽  
Cxcr2 Antagonist

AbstractPeritoneal metastasis is an insidious aspect of colorectal cancer. The aim of the present study was to define mechanisms regulating colon cancer cell adhesion and spread to peritoneal wounds after abdominal surgery. Mice was laparotomized and injected intraperitoneally with CT-26 colon carcinoma cells and metastatic noduli in the peritoneal cavity was quantified after treatment with a CXCR2 antagonist or integrin-αV-antibody. CT-26 cells expressed cell surface chemokine receptors CXCR2, CXCR3, CXCR4 and CXCR5. Stimulation with the CXCR2 ligand, CXCL2, dose-dependently increased proliferation and migration of CT-26 cells in vitro. The CXCR2 antagonist, SB225002, dose-dependently decreased CXCL2-induced proliferation and migration of colon cancer cells in vitro. Intraperitoneal administration of CT-26 colon cancer cells resulted in wide-spread growth of metastatic nodules at the peritoneal surface of laparotomized animals. Laparotomy increased gene expression of CXCL2 at the incisional line. Pretreatment with CXCR2 antagonist reduced metastatic nodules by 70%. Moreover, stimulation with CXCL2 increased CT-26 cell adhesion to extracellular matrix (ECM) proteins in a CXCR2-dependent manner. CT-26 cells expressed the αV, β1 and β3 integrin subunits and immunoneutralization of αV abolished CXCL2-triggered adhesion of CT-26 to vitronectin, fibronectin and fibrinogen. Finally, inhibition of the αV integrin significantly attenuated the number of carcinomatosis nodules by 69% in laparotomized mice. These results were validated by use of the human colon cancer cell line HT-29 in vitro. Our data show that colon cancer cell adhesion and growth on peritoneal wound sites is mediated by a CXCL2-CXCR2 signaling axis and αV integrin-dependent adhesion to ECM proteins.

scholarly journals Novel Anthraquinone Compounds Inhibit Colon Cancer Cell Proliferation via the Reactive Oxygen Species/JNK Pathway

Molecules ◽  
2020 ◽  
Vol 25 (7) ◽  
pp. 1672 ◽  
Author(s):  
Yuying Li ◽  
Fang Guo ◽  
Yingying Guan ◽  
Tinggui Chen ◽  
Kaiqing Ma ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Colon Cancer ◽  
Cancer Cell ◽  
Human Cancer ◽  
Hct116 Cell ◽  
Cell Activity ◽  
Similarity Index ◽  
Reactive Oxygen ◽  
Field Analysis ◽  
Oxygen Species

A series of amide anthraquinone derivatives, an important component of some traditional Chinese medicines, were structurally modified and the resulting antitumor activities were evaluated. The compounds showed potent anti-proliferative activities against eight human cancer cell lines, with no noticeable cytotoxicity towards normal cells. Among the candidate compounds, 1-nitro-2-acyl anthraquinone-leucine (8a) showed the greatest inhibition of HCT116 cell activity with an IC50 of 17.80 μg/mL. In addition, a correlation model was established in a three-dimensional quantitative structure-activity relationship (3D-QSAR) study using Comparative Molecular Field Analysis (CoMFA) and comparative molecular similarity index analysis (CoMSIA). Moreover, compound 8a effectively killed tumor cells by reactive oxygen species (ROS)-JNK activation, causing an increase in ROS levels, JNK phosphorylation, and mitochondrial stress. Cytochrome c was then released into cytoplasm, which, in turn activated the cysteine protease pathway and ultimately induced tumor cell apoptosis, suggesting a potential use of this compound for colon cancer treatment.

Pressure activates colon cancer cell adhesion by inside-out FAK, src and cytoskeletal signaling

2003 ◽  
Vol 124 (4) ◽  
pp. A604
Author(s):  
Vijayalakshmi Thamilselvan ◽  
Richard J. Gilbert ◽  
Marc D. Basson
Keyword(s):  
Colon Cancer ◽  
Cell Adhesion ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Cancer Cell Adhesion ◽  
Inside Out
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