NOD-Like Receptors in Colon Tumorigenesis

10.7178/ig.35 ◽  
2013 ◽  
Vol 2 (2) ◽  
pp. 90 ◽  
Author(s):  
Md. Hasan Zaki ◽  
Keyword(s):  
Colon Tumorigenesis

Mkp-1 is required for chemopreventive activity of butylated hydroxyanisole and resveratrol against colitis-associated colon tumorigenesis

2019 ◽  
Vol 127 ◽  
pp. 72-80 ◽  
Author(s):  
Zhaohong Zheng ◽  
Yeru Chen ◽  
Jianan Huang ◽  
Hong Deng ◽  
Xiuwen Tang ◽  
...  
Keyword(s):  
Butylated Hydroxyanisole ◽  
Colon Tumorigenesis ◽  
Chemopreventive Activity

scholarly journals Claudin-1 overexpression in intestinal epithelial cells enhances susceptibility to adenamatous polyposis coli-mediated colon tumorigenesis

2014 ◽  
Vol 13 (1) ◽  
pp. 167 ◽  
Author(s):  
Jillian L Pope ◽  
Rizwan Ahmad ◽  
Ajaz A Bhat ◽  
Mary K Washington ◽  
Amar B Singh ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Intestinal Epithelial Cells ◽  
Intestinal Epithelial ◽  
Polyposis Coli ◽  
Colon Tumorigenesis

scholarly journals 15-Hydroxyprostaglandin dehydrogenase is an in vivo suppressor of colon tumorigenesis

2006 ◽  
Vol 103 (32) ◽  
pp. 12098-12102 ◽  
Author(s):  
S.-J. Myung ◽  
R. M. Rerko ◽  
M. Yan ◽  
P. Platzer ◽  
K. Guda ◽  
...  
Keyword(s):  
Colon Tumorigenesis

Synbiotic supplementation attenuates the promoting effect of indole-3-carbinol on colon tumorigenesis

2021 ◽  
pp. 1-10
Author(s):  
N.A. de Moura ◽  
B.F.R. Caetano ◽  
L.T. Bidinotto ◽  
M.A.M. Rodrigues ◽  
L.F. Barbisan
Keyword(s):  
Cell Proliferation ◽  
Colon Carcinogenesis ◽  
Basal Diet ◽  
Tumour Volume ◽  
Control Group ◽  
Promoting Effect ◽  
Bifidobacterium Lactis ◽  
Colon Tumorigenesis ◽  
Synbiotic Supplementation ◽  
Well Differentiated

Indole-3 carbinol (I3C) has shown dual effects on the promotion and progression stages of colon carcinogenesis while synbiotics (Syn) have exerted anti-carcinogenic activities in most rodent studies. This study aimed to investigate the effects of I3C given alone or together with a Syn intervention on 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis. All animals were given four subcutaneous DMH injections (4×40 mg/kg bodyweight, twice a week for two weeks) and then received either basal diet (G1), basal diet containing I3C (1g/kg chow) (G2) or basal diet containing I3C+Syn (I3C + inulin 50g/kg chow + Bifidobacterium lactis BB-12®), 2.5×1010 cfu/g of basal diet), (G3) for 21 weeks. Dietary I3C (G2) significantly increased tumour volume and cell proliferation when compared to the DMH control group (G1). Syn intervention (G3) significantly reduced tumour volume and cell proliferation when compared to I3C (G2). The colon tumours found were classified into well-differentiated tubular adenomas or adenocarcinomas. Dietary I3C or I3C+Syn did not significantly affect the incidence and the multiplicity of tumours in comparison with the DMH control group. Furthermore, Syn intervention (G3) increased Gstm1 and reduced Mapk9 gene expression in colonic tumours. The findings of the present study show that the dietary I3C shows a weak promoting activity, while the combination with Syn ameliorates I3C effects.

scholarly journals Destruxin B Suppresses Drug-Resistant Colon Tumorigenesis and Stemness Is Associated with the Upregulation of miR-214 and Downregulation of mTOR/β-Catenin Pathway

Cancers ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 353 ◽  
Author(s):  
Szu-Yuan Wu ◽  
Yan-Jiun Huang ◽  
Yew-Min Tzeng ◽  
Chi-Ying Huang ◽  
Michael Hsiao ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Side Population ◽  
Colon Cancer Cells ◽  
Cancer Stemness ◽  
Colon Cells ◽  
Colon Tumorigenesis ◽  
Tumor Sphere ◽  
Sphere Formation

Background: Drug resistance represents a major challenge for treating patients with colon cancer. Accumulating evidence suggests that Insulin-like growth factor (IGF)-associated signaling promotes colon tumorigenesis and cancer stemness. Therefore, the identification of agents, which can disrupt cancer stemness signaling, may provide improved therapeutic efficacy. Methods: Mimicking the tumor microenvironment, we treated colon cancer cells with exogenous IGF1. The increased stemness of IGF1-cultured cells was determined by ALDH1 activity, side-population, tumor sphere formation assays. Destruxin B (DB) was evaluated for its anti-tumorigenic and stemness properties using cellular viability, colony-formation tests. The mimic and inhibitor of miR-214 were used to treat colon cancer cells to show its functional association to DB treatment. In vivo mouse models were used to evaluate DB’s ability to suppress colon tumor-initiating ability and growth inhibitory function. Results: IGF1-cultured colon cancer cells showed a significant increase in 5-FU resistance and enhanced stemness properties, including an increased percentage of ALDH1+, side-population cells, tumor sphere generation in vitro, and increased tumor initiation in vivo. In support, using public databases showed that increased IGF1 expression was significantly associated with a poorer prognosis in patients with colon cancer. DB, a hexadepsipeptide mycotoxin, was able to suppress colon tumorigenic phenotypes, including colony and sphere formation. The sequential treatment of DB, followed by 5-FU, synergistically inhibited the viability of colon cancer cells. In vivo studies showed that DB suppressed the tumorigenesis by 5-FU resistant colon cells, and in a greater degree when combined with 5-FU. Mechanistically, DB treatment was associated with decreased the mammalian target of rapamycin (mTOR) and β-catenin expression and an increased miR-214 level. Conclusion: We provided evidence of DB as a potential therapeutic agent for overcoming 5-FU resistance induced by IGF1, and suppressing cancer stem-like properties in association with miR-214 regulation. Further investigation is warranted for its translation to clinical application.

scholarly journals Redundant Innate and Adaptive Sources of IL17 Production Drive Colon Tumorigenesis

2016 ◽  
Vol 76 (8) ◽  
pp. 2115-2124 ◽  
Author(s):  
Franck Housseau ◽  
Shaoguang Wu ◽  
Elizabeth C. Wick ◽  
Hongni Fan ◽  
Xinqun Wu ◽  
...  
Keyword(s):  
Colon Tumorigenesis

scholarly journals Sa1706 – Map9 Deficiency Spontaneously Drives Colon Tumorigenesis Through Inducing Chromosome Instability

2019 ◽  
Vol 156 (6) ◽  
pp. S-373
Author(s):  
Shiyan Wang ◽  
Junzhe Huang ◽  
Chuangen Li ◽  
Liuyang Zhao ◽  
Yunfei Zhou ◽  
...  
Keyword(s):  
Chromosome Instability ◽  
Colon Tumorigenesis

scholarly journals Blockade of the LRP16-PKR-NF-κB signaling axis sensitizes colorectal carcinoma cells to DNA-damaging cytotoxic therapy

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Xiaolei Li ◽  
Zhiqiang Wu ◽  
Xiaojing An ◽  
Qian Mei ◽  
Miaomiao Bai ◽  
...  
Keyword(s):  
Colorectal Carcinoma ◽  
Nuclear Factor Kappa B ◽  
Carcinoma Cells ◽  
Therapeutic Resistance ◽  
Cytotoxic Therapy ◽  
Double Stranded Rna ◽  
Colon Tumorigenesis ◽  
Dna Damaging Agents ◽  
Signaling Axis ◽  
Dramatic Shift

Acquired therapeutic resistance by tumors is a substantial impediment to reducing the morbidity and mortality that are attributable to human malignancies. The mechanisms responsible for the dramatic shift between chemosensitivity and chemoresistance in colorectal carcinoma have not been defined. Here, we report that LRP16 selectively interacts and activates double-stranded RNA-dependent kinase (PKR), and also acts as scaffolds to assist the formation of a ternary complex of PKR and IKKβ, prolonging the polymers of ADP-ribose (PAR)-dependent nuclear factor kappa B (NF-κB) transactivation caused by DNA-damaging agents and confers acquired chemoresistance. We also identified a small molecule, MRS2578, which strikingly abrogated the binding of LRP16 to PKR and IKKβ, converting LRP16 into a death molecule and forestalling colon tumorigenesis. Inclusion of MRS2578 with etoposide, versus each drug alone, exhibited synergistic antitumor cytotoxicity in xenografts. Our combinatorial approach introduces a strategy to enhance the efficacy of genotoxicity therapies for the treatment of tumors.

Sign in / Sign up

Export Citation Format

Share Document