scholarly journals X-radiation enhances the collagen type I strap formation and migration potentials of colon cancer cells

Oncotarget ◽  
2016 ◽  
Vol 7 (44) ◽  
pp. 71390-71399 ◽  
Author(s):  
Stephanie Blockhuys ◽  
Na Liu ◽  
Nisha Rani Agarwal ◽  
Annika Enejder ◽  
Vesa Loitto ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Collagen Type ◽  
Collagen Type I ◽  
Type I ◽  
Colon Cancer Cells ◽  
And Migration

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.

SRPK2 promotes the growth and migration of the colon cancer cells

Gene ◽  
2016 ◽  
Vol 586 (1) ◽  
pp. 41-47 ◽  
Author(s):  
Jian Wang ◽  
Hai-Feng Wu ◽  
Wei Shen ◽  
Dong-Yan Xu ◽  
Ting-Yan Ruan ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
And Migration

Kopsanone inhibits proliferation and migration of invasive colon cancer cells

2021 ◽  
Author(s):  
Daniella Paiva Bonfim ◽  
Celso Vataru Nakamura ◽  
João Xavier Araújo Júnior ◽  
Greisiele Lorena Pessini ◽  
Paulo Emílio Correa Leite ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Colon Cancer Cells ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals ADCK1 activates the β-catenin/TCF signaling pathway to promote the growth and migration of colon cancer cells

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Yong Ji ◽  
Yiqian Liu ◽  
Changchun Sun ◽  
Lijiang Yu ◽  
Zhao Wang ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Colony Formation ◽  
Activation Mechanism ◽  
Colon Cancer Cells ◽  
Mechanistic Studies ◽  
T Cell Factor ◽  
And Migration

AbstractAs a result of mutations in the upstream components of the Wnt/β-catenin signaling pathway, this cascade is abnormally activated in colon cancer. Hence, identifying the activation mechanism of this pathway is an urgent need for the treatment of colon cancer. Here, we found an increase in ADCK1 (AarF domain-containing kinase 1) expression in clinical specimens of colon cancer and animal models. Upregulation of ADCK1 expression promoted the colony formation and infiltration of cancer cells. Downregulation of ADCK1 expression inhibited the colony formation and infiltration of cancer cells, in vivo tumorigenesis, migration, and organoid formation. Molecular mechanistic studies demonstrated that ADCK1 interacted with TCF4 (T-cell factor 4) to activate the β-catenin/TCF signaling pathway. In conclusion, our research revealed the functions of ADCK1 in the development of colon cancer and provided potential therapeutic targets.

scholarly journals Invasive Colon Cancer Cells Induce Transdifferentiation of Endothelium to Cancer-Associated Fibroblasts through Microtubules Enriched in Tubulin-β3

2018 ◽  
Vol 20 (1) ◽  
pp. 53 ◽  
Author(s):  
Marta Wawro ◽  
Katarzyna Chojnacka ◽  
Katarzyna Wieczorek-Szukała ◽  
Katarzyna Sobierajska ◽  
Jolanta Niewiarowska
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cancer Associated Fibroblasts ◽  
Colon Cancer Cells ◽  
Migration Ability ◽  
Mesenchymal Transition ◽  
Cytoskeleton Reorganization ◽  
Advanced Stages ◽  
Endothelial To Mesenchymal Transition ◽  
And Migration

Colon cancer, the second leading cause of cancer-related deaths in the world, is usually diagnosed in invasive stages. The interactions between cancer cells and cells located in their niche remain the crucial mechanism inducing tumor metastasis. The most important among those cells are cancer-associated fibroblasts (CAFs), the heterogeneous group of myofibroblasts transdifferentiated from numerous cells of different origin, including endothelium. The endothelial-to-mesenchymal transition (EndMT) is associated with modulation of cellular morphology, polarization and migration ability as a result of microtubule cytoskeleton reorganization. Here we reveal, for the first time, that invasive colon cancer cells regulate EndMT of endothelium via tubulin-β3 upregulation and its phosphorylation. Thus, we concluded that therapies based on inhibition of tubulin-β3 expression or phosphorylation, or blocking tubulin-β3’s recruitment to the microtubules, together with anti-inflammatory chemotherapeutics, are promising means to treat advanced stages of colon cancer.

scholarly journals Cholesteryl butyrate solid lipid nanoparticles inhibit the adhesion and migration of colon cancer cells

2012 ◽  
Vol 166 (2) ◽  
pp. 587-601 ◽  
Author(s):  
R Minelli ◽  
L Serpe ◽  
P Pettazzoni ◽  
V Minero ◽  
G Barrera ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Solid Lipid Nanoparticles ◽  
Lipid Nanoparticles ◽  
Colon Cancer Cells ◽  
Solid Lipid ◽  
And Migration

scholarly journals Effect of a Collagen-Based Compound on Morpho-Functional Properties of Cultured Human Tenocytes

Cells ◽  
2018 ◽  
Vol 7 (12) ◽  
pp. 246 ◽  
Author(s):  
Filippo Randelli ◽  
Alessandra Menon ◽  
Alessio Giai Via ◽  
Manuel Mazzoleni ◽  
Fabio Sciancalepore ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Collagen Type ◽  
Clinical Investigation ◽  
Pain Syndrome ◽  
Collagen Type I ◽  
Type I ◽  
Mrna Levels ◽  
Collagen Turnover ◽  
And Migration ◽  
Proliferation And Migration

Background: Greater Trochanter Pain Syndrome (GTPS) is the main reason for recalcitrant lateral hip pain. Gluteus medius and minimus tendinopathy plays a key role in this setting. An injectable medical compound containing collagen type I (MD-Tissue, Guna) has been produced with the aim to counteract the physiological and pathological degeneration of tendons. In this study we aimed at characterizing the effect of this medical compound on cultured human gluteal tenocytes, focusing on the collagen turnover pathways, in order to understand how this medical compound could influence tendon biology and healing. Methods: Tenocytes were obtained from gluteal tendon fragments collected in eight patients without any gluteal tendon pathology undergoing total hip replacement through an anterior approach. Cell proliferation and migration were investigated by growth curves and wound healing assay, respectively. The expression of genes and proteins involved in collagen turnover were analysed by real-time PCR, Slot blot and SDS-zymography. Results: Our data show that tenocytes cultured on MD-Tissue, compared to controls, have increased proliferation rate and migration potential. MD-Tissue induced collagen type I (COL-I) secretion and mRNA levels of tissue inhibitor of matrix metalloproteinases (MMP)-1 (TIMP-1). Meanwhile, lysyl hydroxylase 2b and matrix metalloproteinases (MMP)-1 and -2, involved, respectively, in collagen maturation and degradation, were not affected. Conclusions: Considered as a whole, our results suggest that MD-Tissue could induce in tenocytes an anabolic phenotype by stimulating tenocyte proliferation and migration and COL-I synthesis, maturation, and secretion, thus favouring tendon repair. In particular, based on its effect on gluteal tenocytes, MD-Tissue could be effective in the discouraging treatment of GTPS. From now a rigorous clinical investigation is desirable to understand the real clinical potentials of this compound.

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