Expression profiles of proliferative and antiapoptotic genes in sporadic and colitis‐related mouse colon cancer models

Švec, Jiří; Ergang, Peter; Mandys, Václav; Kment, Milan; Pácha, Jiřı́

doi:10.1111/j.1365-2613.2009.00698.x

Cited by 14 publications

(5 citation statements)

References 28 publications

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“…Finally, a large upregulation of the Tcf-4 transcript can be also observed in AOM/DSS-induced tumors. [ 70 ]…”

Section: Molecular Features Of the Aom/dss Model And Relevance To Hummentioning

confidence: 99%

“…[ 82 ] Recently, an increased expression of c-Myc and telomerase (TERT) have been observed in foci of high-grade dysplasia/intramucosal carcinoma isolated from AOM/DSS-treated Crj:CD-1 (ICR) mice. [ 62 70 ] Of note, telomerase not only compensates for natural telomere erosion and thus contributes to permanent cell growth, but it is also able to activate progenitor cells by controlling c-Myc- and Wnt-related transcription pathways. [ 82 ]…”

Section: Molecular Features Of the Aom/dss Model And Relevance To Hummentioning

confidence: 99%

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The AOM/DSS murine model for the study of colon carcinogenesis: From pathways to diagnosis and therapy studies

et al. 2011

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Colorectal cancer (CRC) is a major health problem in industrialized countries. Although inflammation-linked carcinogenesis is a well accepted concept and is often observed within the gastrointestinal tract, the underlying mechanisms remain to be elucidated. Inflammation can indeed provide initiating and promoting stimuli and mediators, generating a tumour-prone microenvironment. Many murine models of sporadic and inflammation-related colon carcinogenesis have been developed in the last decade, including chemically induced CRC models, genetically engineered mouse models, and xenoplants. Among the chemically induced CRC models, the combination of a single hit of azoxymethane (AOM) with 1 week exposure to the inflammatory agent dextran sodium sulphate (DSS) in rodents has proven to dramatically shorten the latency time for induction of CRC and to rapidly recapitulate the aberrant crypt foci–adenoma–carcinoma sequence that occurs in human CRC. Because of its high reproducibility and potency, as well as the simple and affordable mode of application, the AOM/DSS has become an outstanding model for studying colon carcinogenesis and a powerful platform for chemopreventive intervention studies. In this article we highlight the histopathological and molecular features and describe the principal genetic and epigenetic alterations and inflammatory pathways involved in carcinogenesis in AOM/DSS–treated mice; we also present a general overview of recent experimental applications and preclinical testing of novel therapeutics in the AOM/DSS model.

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“…Finally, a large upregulation of the Tcf-4 transcript can be also observed in AOM/DSS-induced tumors. [ 70 ]…”

Section: Molecular Features Of the Aom/dss Model And Relevance To Hummentioning

confidence: 99%

Section: Molecular Features Of the Aom/dss Model And Relevance To Hummentioning

confidence: 99%

The AOM/DSS murine model for the study of colon carcinogenesis: From pathways to diagnosis and therapy studies

et al. 2011

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“…In the early stage (from week 1–7), normal crypts are initiated to form foci of aberrant crypts that proliferate by crypt fission to form micro-adenoma. This initial stage is marked by genetic changes that progress with morphological alternation, involving the Wnt/Apc/β-catenin pathway, K-Ras, c-Myc global hypomethylation, iNOS, and COX-2 [ 2 , 3 , 4 , 5 , 6 ]. Following the resolution of acute inflammation, these micro-adenomas will grow and aggregate to form adenomas, adenomatous polyps, and finally adenocarcinomas in the subsequent weeks (the promotion stage).…”

Section: Introductionmentioning

confidence: 99%

Effect of Angelica sinensis Root Extract on Cancer Prevention in Different Stages of an AOM/DSS Mouse Model

Zhao

Kang

Peng

et al. 2017

IJMS

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Angelica sinensis root (ASR) extract was obtained to investigate its effects on colorectal carcinogenesis in different stages of an Azoxymethane/Dextran sodium sulphate (AOM/DSS) model. In this study, we showed that ASR extract administration in the initial stage of the AOM/DSS model had cancer preventive effects with decreasing tumor incidence and a high-grade of intraepithelial neoplasia incidence. With respect to DNA damage, the amounts of 8-oxoguanine and γ-H2AX were suppressed in colon tissue. The balance of apoptosis and proliferation was approaching the normal state. In contrast, ASR extract administration in the promotion stage of the AOM/DSS model accelerated the progression of carcinogenesis. The maximum tumor size reached 49.85 ± 25.04 mm3. High-grade pathological changes were significantly increased. Decreased DNA damage and P53 level reflected the disrupted reactive oxygen species (ROS) concentration in colorectal tissue, which led to an imbalance of proliferative and apoptotic relationships. These findings suggested that the cancer-preventive effect of ASR extract may be stage-dependent in the process of carcinogenesis.

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“…Brain specimens of hypothalamic paraventricular nucleus (PVN), central (CeA) and lateral amygdala (LA), prelimbic (plPFC) and infralimbic prefrontal cortex (ilPFC), hippocampal CA2 and CA3 regions, and ventral (vCA1) and dorsal (dCA1) parts of CA1 region, were prepared by laser microdissection and RNA analysis was performed as previously described, with some modifications [28] . Briefly, coronal brain sections (20 µm) were serially cut with a cryostat at −19°C.…”

Section: Methodsmentioning

confidence: 99%

Regulation of 11β-Hydroxysteroid Dehydrogenase Type 1 and 7α-Hydroxylase CYP7B1 during Social Stress

et al. 2014

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11β-hydroxysteroid dehydrogenase type 1 (11HSD1) is an enzyme that amplifies intracellular glucocorticoid concentration by the conversion of inert glucocorticoids to active forms and is involved in the interconversion of 7-oxo- and 7-hydroxy-steroids, which can interfere with the activation of glucocorticoids. The presence of 11HSD1 in the structures of the hypothalamic-pituitary-adrenal (HPA) axis suggests that this enzyme might play a role in the regulation of HPA output. Here we show that the exposure of Fisher 344 rats to mild social stress based on the resident-intruder paradigm increased the expression of 11HSD1 and CYP7B1, an enzyme that catalyzes 7-hydroxylation of steroids. We found that social behavioral profile of intruders was significantly decreased whereas their plasma levels of corticosterone were increased more than in residents. The stress did not modulate 11HSD1 in the HPA axis (paraventricular nucleus, pituitary, adrenal cortex) but selectively upregulated 11HSD1 in some regions of the hippocampus, amygdala and prelimbic cortex. In contrast, CYP7B1 was upregulated not only in the hippocampus and amygdala but also in paraventricular nucleus and pituitary. Furthermore, the stress downregulated 11HSD1 in the thymus and upregulated it in the spleen and mesenteric lymphatic nodes whereas CYP7B1 was upregulated in all of these lymphoid organs. The response of 11HSD1 to stress was more obvious in intruders than in residents and the response of CYP7B1 to stress predominated in residents. We conclude that social stress induces changes in enzymes of local metabolism of glucocorticoids in lymphoid organs and in brain structures associated with the regulation of the HPA axis. In addition, the presented data clearly suggest a role of 11HSD1 in modulation of glucocorticoid feedback of the HPA axis during stress.

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Expression profiles of proliferative and antiapoptotic genes in sporadic and colitis‐related mouse colon cancer models

Cited by 14 publications

References 28 publications

The AOM/DSS murine model for the study of colon carcinogenesis: From pathways to diagnosis and therapy studies

The AOM/DSS murine model for the study of colon carcinogenesis: From pathways to diagnosis and therapy studies

Effect of Angelica sinensis Root Extract on Cancer Prevention in Different Stages of an AOM/DSS Mouse Model

Regulation of 11β-Hydroxysteroid Dehydrogenase Type 1 and 7α-Hydroxylase CYP7B1 during Social Stress

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