Clostridium butyricum, a Butyrate-Producing Probiotic, Inhibits Intestinal Tumor Development Through Modulating Wnt Signaling and Gut Microbiota

2019 ◽  
Author(s):  
Danfeng Chen ◽  
Duochen Jin ◽  
Shumin Huang ◽  
Jingyi Wu ◽  
Mengque Xu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Wnt Signaling ◽  
Tumor Development ◽  
Clostridium Butyricum ◽  
Intestinal Tumor

Clostridium butyricum, a butyrate-producing probiotic, inhibits intestinal tumor development through modulating Wnt signaling and gut microbiota

2020 ◽  
Vol 469 ◽  
pp. 456-467 ◽  
Author(s):  
Danfeng Chen ◽  
Duochen Jin ◽  
Shumin Huang ◽  
Jingyi Wu ◽  
Mengque Xu ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Wnt Signaling ◽  
Tumor Development ◽  
Clostridium Butyricum ◽  
Intestinal Tumor

scholarly journals The Effects of Berberine on the Gut Microbiota in Apc min/+ Mice Fed with a High Fat Diet

Molecules ◽  
2018 ◽  
Vol 23 (9) ◽  
pp. 2298 ◽  
Author(s):  
Huan Wang ◽  
Lingnan Guan ◽  
Jing Li ◽  
Maode Lai ◽  
Xiaodong Wen
Keyword(s):  
Colorectal Cancer ◽  
16S Rrna ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Tumor Development ◽  
Intestinal Tumor ◽  
High Fat ◽  
Rrna Sequencing ◽  
Hematoxylin And Eosin ◽  
Hematoxylin And Eosin Staining

Background: Berberine (BBR) has been extensively reported to inhibit colorectal cancer (CRC) development, though its bioavailability is poor. Nowadays, an increasing number of studies have shown that BBR significantly accumulates in the intestines and could regulate gut microbiota in obesity. The purpose of this study was to further explore the effects of BBR on gut microbiota in Apc min/+ mice receiving a high fat diet (HFD). Methods: Apc min/+ mice received either HFD alone or HFD and BBR for 12 weeks. The intestinal tissues were collected to evaluate the efficiency of BBR on neoplasm development by hematoxylin and eosin staining. Meanwhile, immunohistochemistry was conducted to investigate the effects of BBR on cyclin D1 and β-catenin in colon tissues. Fecal samples were subjected to 16S rRNA sequencing. Results: BBR significantly reduced intestinal tumor development and altered the structure of gut microbiota in Apc min/+ mice fed with an HFD. At the phylum level, it was able to significantly inhibit the increase in Verrucomicrobia. At the genus level, it was able to suppress Akkermansia and elevate some short chain fat acid (SCFA)-producing bacteria. Conclusions: BBR significantly alleviated the development of CRC in Apc min/+ mice fed with HFD and restored the enteric microbiome community.

scholarly journals Gut Microbiota, Fusobacteria, and Colorectal Cancer

Diseases ◽  
2018 ◽  
Vol 6 (4) ◽  
pp. 109 ◽  
Author(s):  
Dervla Kelly ◽  
Liying Yang ◽  
Zhiheng Pei
Keyword(s):  
Colorectal Cancer ◽  
Gut Microbiota ◽  
Inflammatory Responses ◽  
Tumor Development ◽  
Host Responses ◽  
Future Research ◽  
Bacterial Microbiota ◽  
Promote Tumor Growth ◽  
Tumor Environment ◽  
Protective Strategies

The gut microbiota has emerged as an environmental contributor to colorectal cancer (CRC) in both animal models and human studies. It is now generally accepted that bacteria are ubiquitous colonizers of all exposed human body surfaces, including the entire alimentary tract (5). Recently, the concept that a normal bacterial microbiota is essential for the development of inflammation-induced carcinoma has emerged from studies of well-known colonic bacterial microbiota. This review explores the evidence for a role of fusobacteria, an anaerobic gram-negative bacterium that has repeatedly been detected at colorectal tumor sites in higher abundance than surrounding histologically normal tissue. Mechanistic studies provide insight on the interplay between fusobacteria, other gut microbiota, barrier functions, and host responses. Studies have shown that fusobacteria activate host inflammatory responses designed to protect against pathogens that promote tumor growth. We discuss how future research identifying the pathophysiology underlying fusobacteria colon colonization during colorectal cancer may lead to new therapeutic targets for cancer. Furthermore, disease-protective strategies suppressing tumor development by targeting the local tumor environment via bacteria represent another exciting avenue for researchers and are highlighted in this review.

Molecular Profiling of Isolated Histological Components of Wilms Tumor Implicates a Common Role for the Wnt Signaling Pathway in Kidney and Tumor Development

Oncology ◽  
2008 ◽  
Vol 75 (1-2) ◽  
pp. 81-91 ◽  
Author(s):  
Mariana Maschietto ◽  
Beatriz de Camargo ◽  
Helena Brentani ◽  
Paul Grundy ◽  
Simone T. Sredni ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Signaling Pathway ◽  
Wilms Tumor ◽  
Wnt Signaling Pathway ◽  
Tumor Development ◽  
Molecular Profiling

scholarly journals 619 – Myeloid Calcineurin in the Control of Immune Checkpoint Inhibition in Intestinal Tumor Development

2019 ◽  
Vol 156 (6) ◽  
pp. S-128-S-129
Author(s):  
Kenneth Peuker ◽  
Anne Strigli ◽  
Lea Juznic ◽  
Liz Matthiesen ◽  
Michael U. Koch ◽  
...  
Keyword(s):  
Immune Checkpoint ◽  
Tumor Development ◽  
Intestinal Tumor ◽  
Checkpoint Inhibition ◽  
Immune Checkpoint Inhibition

scholarly journals Osteopontin Deficiency Suppresses Intestinal Tumor Development in Apc-Deficient Min Mice

2017 ◽  
Vol 18 (5) ◽  
pp. 1058 ◽  
Author(s):  
Rikako Ishigamori ◽  
Masami Komiya ◽  
Shinji Takasu ◽  
Michihiro Mutoh ◽  
Toshio Imai ◽  
...  
Keyword(s):  
Tumor Development ◽  
Intestinal Tumor

A new CRISPR mediated intestinal tumor mouse model targeting four canonical tumor suppressor genes.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e16064-e16064
Author(s):  
Hajime Kashima ◽  
Daniel Veronese-Paniagua ◽  
Anthony Fischer ◽  
Blair Madison ◽  
Deborah Rubin
Keyword(s):  
Tumor Suppressor ◽  
Mouse Model ◽  
Tumor Suppressor Genes ◽  
Rapid Development ◽  
Tumor Development ◽  
Intestinal Tumor ◽  
Intestinal Tumors ◽  
Suppressor Genes ◽  
Intestinal Tumorigenesis ◽  
Guide Rnas

e16064 Background: Mouse models of intestinal tumorigenesis have been developed and many of them involve mutations in the Apc gene. However, human intestinal tumors contain multiple additional sporadic mutations in tumor suppressor genes (TSGs). Our goal is to develop a novel mouse model of intestinal tumorigenesis that can recapitulate the natural history of mutations in diverse stages of tumor development. Methods: We used multiple guide RNAs to achieve random mutations in the canonical TSGs, Apc, Pten, Smad4, and Tp53. We generated transgenic (PPAS) mice that constitutively express the appropriate guide RNAs. Moreover, we achieved inducible Cas9 expression in icCas9N mice intestine using the Villin promoter to drive both a doxycycline-dependent activator and a doxycycline-inactivated repressor. We fed the doxycycline chow to PPAS:icCas9 double transgenic mice from the age of 6 to 8 weeks, and harvested intestine at 12 weeks. Results: We examined seven PPAS;icCas9 mice, and detected intestinal tumors in all the mice. Two mice had small intestinal tumor, three mice had colonic tumor, and two mice had tumors in both small and large intestine. The average number of tumors were 0.86, 1.57, 2.43 in small intestine, colon, and both respectively. We analyzed mutations in 11 tumors in 6 mice. The mutation patterns of Apc, Pten, Smad4 and Tp53 in tumors shared three distinct patterns. One was characterized by mutations in all four TSGs (n = 9). The second showed mutation in APC and Smad4 and Pten (n = 1). The third showed mutation only in Tp53 (n = 1). Normal intestine and colon in PPAS:icCas9 mice had no mutations. Conclusions: This model provides a powerful platform for modeling intestinal tumorigenesis driven by the canonical signaling pathway which are commonly dysregulated in colon cancer. This model provides a means for rapid development of intestinal tumors in mice, enabling an investigation of the relationship between novel candidate regulators of tumorigenesis and the canonical signaling pathways regulated by these four common TSGs. [Table: see text]

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