scholarly journals Plasma-membrane-associated sialidase (NEU3) differentially regulates integrin-mediated cell proliferation through laminin- and fibronectin-derived signalling

2006 ◽  
Vol 394 (3) ◽  
pp. 647-656 ◽  
Author(s):  
Kengo Kato ◽  
Kiyoto Shiga ◽  
Kazunori Yamaguchi ◽  
Keiko Hata ◽  
Toshimitsu Kobayashi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Plasma Membrane ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Molecular Mechanisms ◽  
Human Colon ◽  
Human Colon Cancer ◽  
Laminin 5 ◽  
Colon Cancers ◽  
Integrin Β4

We have found previously that human plasma-membrane-associated sialidase (NEU3), a key glycosidase for ganglioside degradation, was markedly up-regulated in human colon cancers, with an involvement in suppression of apoptosis. To elucidate the molecular mechanisms underlying increased NEU3 expression, in the present study we investigated its role in cell adhesion of human colon cancer cells. DLD-1 cells transfected with NEU3 exhibited increased adhesion to laminins and consequent cell proliferation, but decreased cell adhesion to fibronectin and collagens I and IV, compared with control cells. When triggered by laminins, NEU3 clearly stimulated phosphorylation of FAK (focal adhesion kinase) and ERK (extracellular-signal-regulated kinase), whereas there was no activation on fibronectin. NEU3 markedly enhanced tyrosine phosphorylation of integrin β4 with recruitment of Shc and Grb-2 only on laminin-5, and NEU3 was co-immunoprecipitated by an anti-(integrin β4) antibody, suggesting that association of NEU3 with integrin β4 might facilitate promotion of the integrin-derived signalling on laminin-5. In addition, the promotion of phosphorylation of integrin β1 and ILK (integrin-linked kinase) was also observed on laminins. GM3 depletion as the result of NEU3 overexpression, assessed by TLC, appeared to be one of the causes of the increased adhesion on laminins and, in contrast, of the decreased adhesion on fibronectin – NEU3 probably having bimodal effects. These results indicate that NEU3 differentially regulates cell proliferation through integrin-mediated signalling depending on the extracellular matrix and, on laminins, NEU3 did indeed activate molecules often up-regulated in carcinogenesis, which may cause an acceleration of the malignant phenotype in cancer cells.

Inhibition of N-linked glycosylation by tunicamycin induces E-cadherin-mediated cell–cell adhesion and inhibits cell proliferation in undifferentiated human colon cancer cells

2010 ◽  
Vol 68 (1) ◽  
pp. 227-238 ◽  
Author(s):  
Julio Cesar Madureira de Freitas Junior ◽  
Bárbara Du Rocher D’Aguiar Silva ◽  
Waldemir Fernandes de Souza ◽  
Wallace Martins de Araújo ◽  
Eliana Saul Furquim Werneck Abdelhay ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cell Adhesion ◽  
Cancer Cells ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells ◽  
E Cadherin ◽  
Cell Cell

scholarly journals Cancer Preventive Effect of a Novel High Phenolic Sorghum Bran on Human Colon Cancer Cells (P05-008-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Seong-Ho Lee ◽  
Jihye Lee ◽  
Thomas Herald ◽  
Sarah Cox ◽  
Leela Noronha ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Citric Acid ◽  
Cancer Cells ◽  
Human Colon ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Sorghum Bran ◽  
Human Colon Cancer Cells

Abstract Objectives Colon cancer is one of leading causes of cancer mortality worldwide. Sorghum is the fifth most largely cultivated crop for human diet in the world. Most sorghum varieties contain high content of phenolic compounds. The objective of the current study is to evaluate the anti-cancer properties of a novel high phenolic sorghum bran extract prepared under 70% ethanol with 5% citric acid solvent. Methods High phenolic sorghum, accession number PI570481, was grown in Puerto Vallarta, Mexico winter nursery during the 2018 and high phenolic sorghum bran extract was prepared using 70% ethanol with 5% citric acid solvent at room temperature for 2 hours. Human colon cancer cell lines (HCT15, SW480, HCT116 and HT-29) were treated with different doses of high phenolic sorghum bran extract. Cell proliferation and apoptosis was measured using MTS assay and Alexa Fluor 488 Annexin V/Dead Cell Apoptosis system, respectively. Distribution of cell cycle was measured Texas Red channel using BD LSRFortessa system. Cell migration and invasion was measured using wound healing assay and Matrigel, respectively. The luciferase activity of reporter genes was measured using a dual-luciferase assay and Western blot was performed to measure expression of cancer phenotype-associated proteins. Results Cell proliferation was inhibited and apoptosis was induced in the human colon cancer cells treated with high phenolic sorghum bran extract in a dose-dependent manner. High phenolic sorghum bran extract led to S phage arrest. Cell migration and invasion was also repressed in the human colon cancer cells treated with high phenolic sorghum bran extract. The change of cancer phenotypes was associated with up- or down-regulation of regulatory genes. Conclusions The present study expands our understanding on the potential use of high phenolic sorghum bran for prevention of human colon cancer. Funding Sources Cooperative Agreement grant from USDA-ARS to S-HL.

Cocoplum (Chrysobalanus icaco L.) anthocyanins exert anti-inflammatory activity in human colon cancer and non-malignant colon cells

2017 ◽  
Vol 8 (1) ◽  
pp. 307-314 ◽  
Author(s):  
Vinicius P. Venancio ◽  
Paula A. Cipriano ◽  
Hyemee Kim ◽  
Lusânia M. G. Antunes ◽  
Stephen T. Talcott ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Human Colon ◽  
Inflammatory Activity ◽  
Human Colon Cancer ◽  
Colon Cells ◽  
Anti Inflammatory

Cocoplum anthocyanins reduced cell proliferation in cancer cells and decreased inflammation in both non-malignant and cancer cells.

scholarly journals β-Catenin/TCF4 Complex-Mediated Induction of the NRF3 (NFE2L3) Gene in Cancer Cells

2019 ◽  
Vol 20 (13) ◽  
pp. 3344 ◽  
Author(s):  
Shiori Aono ◽  
Ayari Hatanaka ◽  
Atsushi Hatanaka ◽  
Yue Gao ◽  
Yoshitaka Hippo ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Glucose Transporter ◽  
Human Colon ◽  
Human Colon Cancer ◽  
Genome Database ◽  
Related Transcription Factor ◽  
Cancer Tissues

Remarkable upregulation of the NRF2 (NFE2L2)-related transcription factor NRF3 (NFE2L3) in several cancer tissues and its correlation with poor prognosis strongly suggest the physiological function of NRF3 in tumors. Indeed, we had recently uncovered the function of NRF3, which promotes cancer cell proliferation by p53 degradation via the 20S proteasome. Nevertheless, the molecular mechanism underlying the induction of NRF3 gene expression in cancer cells is highly elusive. We herein describe that NRF3 upregulation is induced by the β-catenin/TCF4 complex in colon cancer cells. We first confirmed high NRF3 mRNA expression in human colon cancer specimens. The genome database indicated that the human NRF3 gene possesses a species-conserved WRE sequence (TCF/LEF consensus element), implying that the β-catenin/TCF complex activates NRF3 expression in colon cancer. Consistently, we observed that the β-catenin/TCF4 complex mediates NRF3 expression by binding directly to the WRE site. Furthermore, inducing NRF3 activates cell proliferation and the expression of the glucose transporter GLUT1. The existence of the β-catenin/TCF4-NRF3 axis was also validated in the intestine and organoids of Apc-deficient mice. Finally, the positive correlation between NRF3 and β-catenin target gene expression strongly supports our conclusion. Our findings clearly demonstrate that NRF3 induction in cancer cells is controlled by the Wnt/β-catenin pathway.

scholarly journals Inhibition of Stearoyl-CoA Desaturase-1 Activity Suppressed SREBP Signaling in Colon Cancer Cells and Their Spheroid Growth

2019 ◽  
Vol 1 (1) ◽  
pp. 191-200 ◽  
Author(s):  
Xian-Yang Qin ◽  
Soichi Kojima
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cholesterol Metabolism ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Spheroid Growth ◽  
Stearoyl Coa Desaturase

Unsaturated fatty acids are critical in promoting colon tumorigenesis and its stemness. Stearoyl-CoA desaturase-1 (SCD1) is a rate-limiting lipid desaturase associated with colon cancer cell proliferation and metastasis control. This study aims to evaluate the effects of SCD1 inhibition on colon cancer spheroid growth in a three-dimensional cell culture system. An analysis of clinical data showed that increased SCD1 gene expression in colon tumors was negatively correlated with the prognosis. A chemical inhibitor of SCD1, CAY10566, inhibited the growth of colon cancer cells in both monolayer and sphere cultures. In addition, oleic acid administration—a monounsaturated fatty acid generated by the action of SCD1—prevented the suppression of sphere formation by CAY10566. RNA-sequencing data from 382 colon tumor patient samples obtained from the Cancer Genome Atlas database showed that 806 genes were SCD1-associated genes in human colon cancer. Correlation analysis identified the master regulator of lipid homeostasis sterol regulatory element-binding protein 2 (SREBP2) as a prominent transcription factor, whose expression was positively correlated with SCD1 in human colon cancer. SCD1 knockdown using siRNA in colon cancer samples, suppressed SREBP2 gene expression, providing direct evidence that SREBP signaling is under the control of SCD1 in these cells. Pathway analysis in the Ingenuity Pathways Analysis platform showed that SCD1 expression positively correlated with genes involved in multiple pathways, including lipid synthesis and incorporation, cell proliferation, and tissue tumorigenesis. Further network analysis revealed a central role for Myc in the network hierarchy of the SCD1-correlated genes. These findings suggested that SCD1 inhibition would be an effective strategy for suppressing colon cancer spheroid growth, partly through downregulating SREBP-mediated lipid and cholesterol metabolism and Myc signaling.

scholarly journals Oyaksungisan, a Traditional Herbal Formula, Inhibits Cell Proliferation by Induction of AutophagyviaJNK Activation in Human Colon Cancer Cells

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Nam-Hui Yim ◽  
Young Pil Jung ◽  
Aeyung Kim ◽  
Choong Je Ma ◽  
Won-Kyung Cho ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Human Colon ◽  
Mitogen Activated Protein Kinase ◽  
Herbal Formula ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Human Colon Cancer Cells ◽  
Hct116 Cells

Oyaksungisan (OY) is a traditional herbal formula broadly used to treat beriberi, vomiting, diarrhea, and circulatory disturbance in Asian countries from ancient times. The effect of OY on cancer, however, was not reported until now. In this study, we have demonstrated that OY inhibits cell proliferation and induces cell deathviamodulating the autophagy on human colon cancer cells. In HCT116 cells, OY increased the ratio of LC3-II/LC3-I, a marker of autophagy, and treatment with 3-MA, an inhibitor of autophagy, and considerably reduced the formation of autophagosomes. In addition, OY regulated mitogen-activated protein kinase (MAPK) cascades; especially, JNK activation was closely related with autophagy effect by OY in HCT116 cells. Our results indicate that autophagy induction is responsible for the antiproliferative effect by OY, despite the weak apoptosis induction in HCT116 cells. In conclusion, OY might have a potential to be developed as an herbal anticancer remedy.

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