Current overview of colitis-associated colorectal cancer

Sobczak, Marcin; Wlazłowski, Marcin; Zatorski, Hubert; Sałaga, Maciej; Fichna, Jakub

doi:10.2478/s11535-014-0345-7

Cited by 5 publications

(4 citation statements)

References 56 publications

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“…Colitis-Associated Carcinogenesis (CAC) ranks the third most frequently diagnosed cancer and the second leading cause of cancer death in developed countries [ 1 , 2 ]. Inflammatory bowel disease (IBD), known as a group of disorders characterized by recurring inflammation of the lower intestine, is considered as an important factor in the progression of CAC, emphasizing that patients suffering from IBD, such as Crohn’s disease and Ulcerative colitis (UC), are at a high risk for CAC [ 3 , 4 ].…”

Section: Introductionmentioning

confidence: 99%

Flavonoids Extracted from Licorice Prevents Colitis-Associated Carcinogenesis in AOM/DSS Mouse Model

Huo

Dongyu

Gao

et al. 2016

IJMS

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Inflammatory bowel disease (IBD) is generally considered as a major risk factor in the progression of colitis-associated carcinogenesis (CAC). Thus, it is well accepted that ameliorating inflammation creates a potential to achieve an inhibitory effect on CAC. Licorice flavonoids (LFs) possess strong anti-inflammatory activity, making it possible to investigate its pharmacologic role in suppressing CAC. The purpose of the present study was to evaluate the anti-tumor potential of LFs, and further explore the underlying mechanisms. Firstly, an azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced mouse model was established and administered with or without LFs for 10 weeks, and then the severity of CAC was examined macroscopically and histologically. Subsequently, the effects of LFs on expression of proteins associated with apoptosis and proliferation, levels of inflammatory cytokine, expression of phosphorylated-Janus kinases 2 (p-Jak2) and phosphorylated-signal transducer and activator of transcription 3 (p-Stat3), and activation of nuclear factor-κB (NFκB) and P53 were assessed. We found that LFs could significantly reduce tumorigenesis induced by AOM/DSS. Further study revealed that LFs treatment substantially reduced activation of NFκB and P53, and subsequently suppressed production of inflammatory cytokines and phosphorylation of Jak2 and Stat3 in AOM/DSS-induced mice. Taken together, LFs treatment alleviated AOM/DSS induced CAC via P53 and NFκB/IL-6/Jak2/Stat3 pathways, highlighting the potential of LFs in preventing CAC.

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Section: Introductionmentioning

confidence: 99%

Flavonoids Extracted from Licorice Prevents Colitis-Associated Carcinogenesis in AOM/DSS Mouse Model

Huo

Dongyu

Gao

et al. 2016

IJMS

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“…The infiltrating inflammatory cells produce a variety of pro-inflammatory cytokines, chemokines, and growth factors to promote an immune response. However, excessive immune responses lead to tissue damage and tumor development ( Sobczak et al, 2014 ; Li et al, 2017 ). Furthermore, parainflammation, which is a low level of inflammation that is intermediate between homeostasis and classical inflammation, is commonly widespread in different cancers, including CRC ( Aran et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

A Potential Role for Integrin-Linked Kinase in Colorectal Cancer Growth and Progression via Regulating Senescence and Immunity

et al. 2021

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Integrin-linked kinase (ILK) has been implicated as a molecular driver and mediator in both inflammation and tumorigenesis of the colon. ILK functions as an adaptor and mediator protein linking the extracellular matrix with downstream signaling pathways. ILK is broadly expressed in many human tissues and cells. It is also overexpressed in many cancers, including colorectal cancer (CRC). Inflammation, as evidenced by inflammatory bowel disease (IBD), is one of the highest risk factors for initiating CRC. This has led to the hypothesis that targeting ILK therapeutically could have potential in CRC, as it regulates different cellular processes associated with CRC development and progression as well as inflammation in the colon. A number of studies have indicated an ILK function in senescence, a cellular process that arrests the cell cycle while maintaining active metabolism and transcription. Senescent cells produce different secretions collectively known as the senescence-associated secretory phenotype (SASP). The SASP secretions influence infiltration of different immune cells, either positively for clearing senescent cells or negatively for promoting tumor growth, reflecting the dual role of senescence in cancer. However, a role for ILK in senescence and immunity in CRC remains to be determined. In this review, we discuss the possible role for ILK in senescence and immunity, paying particular attention to the relevance of ILK in CRC. We also examine how activating Toll-like receptors (TLRs) and their agonists in CRC could trigger immune responses against cancer, as a combination therapy with ILK inhibition.

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“…5 Accumulating evidence indicates that genomic alterations, oxidative stress, cytokines, and inflammatory transcription factors may have crucial roles in the development of CACRC. 6 In chronic inflammation, inflammatory cells produce a variety of pro-inflammatory cytokines and growth factors that stimulate tumor cell proliferation. 7 Macrophages and dendritic cells initiate innate immune responses by secreting pro-inflammatory cytokines, such as IL-1α, IL-6, IL-1, TNF-α, IFN-α, and KC.…”

mentioning

confidence: 99%

“…5 However, exaggerated immune responses typically produce excessive cytokines and chemokines, which most likely result in colon tissue damage and tumorigenesis. 6 Therefore, appropriate regulation of immune responses is imperative during clinical treatment of CACRC. Investigations into the mechanisms of CACRC development and progression will undoubtedly provide new insights into the identification of effective therapeutic strategies.…”

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confidence: 99%

Berberine inhibits colitis-associated tumorigenesis via suppressing inflammatory responses and the consequent EGFR signaling-involved tumor cell growth

Zhang

Liu

et al. 2017

Laboratory Investigation

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The anti-inflammatory and anti-tumor effects of berberine, a traditional Chinese medicine, were separately discovered in pathological intestinal tissues. However, whether the anti-inflammatory effect of berberine contributes to its anti-tumor effect on colitis-associated colorectal cancer (CACRC) remains unknown. In the present study, we found that berberine effectively inhibited colitis-associated tumorigenesis and colonic epithelium hyperproliferation in dextran sulfate sodium (DSS)-treated Apc mice. A mechanistic study identified that these inhibitory effects of berberine occurred through blocking interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) expression in colonic macrophages. An in vitro study on cell lines identified that berberine treatment of Raw 264.7 macrophages resulted in conditioned media with fewer proliferative effects on a cell line with a heterozygous Apc mutation (Immorto-Min colonic epithelium, IMCE). EGFR-ERK signaling act downstream of berberine/pro-inflammatory cytokines axis to regulate CACRC cell proliferation. Furthermore, in vivo administration of IL-6 to DSS-treated Apc mice effectively weakened the inhibitory effects of berberine on tumorigenesis and EGFR-ERK signaling in colon tissues. Altogether, the results of our studies have revealed that berberine inhibits the development of CACRC by interfering with inflammatory response-driven EGFR signaling in tumor cell growth. The findings of this study support the possibility that berberine and other anti-inflammatory drugs may be beneficial in the treatment of CACRC.

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Current overview of colitis-associated colorectal cancer

Cited by 5 publications

References 56 publications

Flavonoids Extracted from Licorice Prevents Colitis-Associated Carcinogenesis in AOM/DSS Mouse Model

Flavonoids Extracted from Licorice Prevents Colitis-Associated Carcinogenesis in AOM/DSS Mouse Model

A Potential Role for Integrin-Linked Kinase in Colorectal Cancer Growth and Progression via Regulating Senescence and Immunity

Berberine inhibits colitis-associated tumorigenesis via suppressing inflammatory responses and the consequent EGFR signaling-involved tumor cell growth

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