p53 expression in patients with ulcerative colitis - associated with dysplasia and carcinoma: a systematic meta-analysis

Lü, Xiaohong; Yu, Yuanjie; Sheng, T. T.

doi:10.1186/s12876-017-0665-y

Cited by 22 publications

(21 citation statements)

References 42 publications

(45 reference statements)

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“…As a tumor suppressor, p53 plays a crucial role in the cell cycle, apoptosis and senescence, and is highly expressed in patients with UC-CRC. 42 In our study, the expression of p53 was significantly enhanced by AOM/DSS in mice. p53 is normally low-expressed in cells and rapidly degraded.…”

Section: Discussionsupporting

confidence: 51%

<p>miR-370-3p Alleviates Ulcerative Colitis-Related Colorectal Cancer in Mice Through Inhibiting the Inflammatory Response and Epithelial-Mesenchymal Transition</p>

Lin¹,

Wang²,

Qu³

et al. 2020

DDDT

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Introduction: Ulcerative colitis (UC) is a chronic and inflammatory bowel disease. UCassociated colorectal cancer (UC-CRC) is one of the most severe complications of long-standing UC. In the present study, we explored the effects of miR-370-3p on UC-CRC in vivo and investigated its underlying mechanisms in vivo and in vitro. Methods: Azoxymethane (AOM) and dextran sodium sulfate (DSS) were used to induce UC-CRC in C57BL/6 mice. AOM/DSS-induced mice were treated with 5×10 8 pfu miR-370-3p overexpressing-adenovirus via tail-vein injection every two weeks. Results: We found that miR-370-3p significantly improved the body weights and survival rates and inhibited the tumorigenesis of UC-CRC in AOM/DSS mice. Mechanically, miR-370-3p inhibited AOM/DSS-induced inflammatory response by decreasing tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) through targeting toll-like receptor 4 (TLR4), as demonstrated by down-regulation of TLR4, cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and phosphorylated epidermal growth factor receptor (pEGFR). miR-370-3p decreased the expression of tumor-associated proteins, including p53, β-catenin, and ki67 in AOM/DSS-treated mice. Additionally, miR-370-3p remarkably inhibited epithelialmesenchymal transition (EMT) via increasing E-cadherin expression and reducing N-cadherin and Vimentin expression in vivo. Further studies showed that miR-370-3p repressed proliferation and EMT of colon cancer cells in vitro. Moreover, we proved that miR-370-3p decreased the expression of tumor-associated proteins and reversed EMT by regulating β-catenin in colon cancer cells. Conclusion: Taken together, miR-370-3p alleviated UC-CRC by inhibiting the inflammatory response and EMT in mice, which suggested miR-370-3p as a novel potential target for UC-CRC therapy.

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Section: Discussionsupporting

confidence: 51%

<p>miR-370-3p Alleviates Ulcerative Colitis-Related Colorectal Cancer in Mice Through Inhibiting the Inflammatory Response and Epithelial-Mesenchymal Transition</p>

Lin¹,

Wang²,

Qu³

et al. 2020

DDDT

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“…The cause of UC-CRC is considered to be the accumulation of inflammatory changes associated with colonic epithelial injury, repair, and regeneration, and the disease is believed to occur in an inflammation-dysplasiacarcinoma sequence. To ascertain tumor aggressiveness in the context of this sequence, p53 expression has been used (3,4), However, there is a need for other biomarkers that can predict the degree of tumor malignancy.…”

mentioning

confidence: 99%

Immunohistochemical Expression of CD133 and LGR5 in Ulcerative Colitis-associated Colorectal Cancer and Dysplasia

Kazama

Kishikawa

Tanaka

et al. 2019

In Vivo

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Background/Aim: Cluster of differentiation 133 (CD133) and leu cine-rich orphan G-protein-coupled receptor 5 (LGR5) are the most putative stem cell markers for colorectal cancer (CRC), and are associated with poor prognosis of patients with CRC. However, the role of CD133 and LGR5 in the inflammation-dysplasia-carcinoma sequence has not been fully elucidated. We examined the expression of CD133 and LGR5 in ulcerative colitisassociated CRC (UC-CRC; n=20) and UC-associated colorectal dysplasia (n=16) by immunohistochemistry. Results: The rate of CD133-positive cases in UC-CRC was significantly higher than that in dysplasia (p=0.026), but that of LGR5 expression was not. Moreover, LGR5 expression was significantly positively associated with p53 expression (p=0.03), whereas CD133 expression positively correlated with p53 expression, but not significantly (p=0.10). Conclusion: CD133 may play an important role in tumor development in the context of the inflammationdysplasia-carcinoma sequence. LGR5-positive cancer stem cells may play a critical role in the development of UC-CRC, particularly upon loss of p53 function.

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“…Lu et al have shown in their meta-analysis that p53 expression was positive in cases of UC associated with carcinoma and dysplasia (5). The frequency of anti-p53 Abs in patients with tumors is strictly correlated with the frequency of p53 mutations (16).…”

Section: Discussionmentioning

confidence: 99%

“…These mutations result in the accumulation of the p53 protein, which causes p53 overexpression in tissue. There have been many reports of p53 overexpression in cases of ulcerative colitisassociated colorectal cancer (CAC) (5).…”

mentioning

confidence: 99%

Uselessness of Serum p53 Antibody for Detecting Colitis-associated Cancer in the Era of Immunosuppressive Therapy

Toritani

Kimura

Kunisaki

et al. 2020

In Vivo

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Background/Aim: The present study examined the utility of serum p53 antibody (Ab) for detecting colitisassociated cancer (CAC) in the era of immunosuppressive therapy. Patients and Methods: Two hundred and fifty patients were analyzed, 219 had no carcinoma or dysplasia (Group non-CAC), and 31 had carcinoma or dysplasia (Group CAC). Serum p53 Abs were detected with an enzyme-linked immunosorbent assay. Immunohistochemical detection was performed in Group CAC. Results: Immunosuppressive therapy was performed in 98.1% of Group non-CAC and 80.6% of Group CAC. There were no differences in serum p53 Abs positivity between p=0.30). p53 staining positivity was noted in 90.3% of Group CAC, and the rate of serum p53 positivity was significantly lower in patients with immunosuppressive therapy than in those without in Group CAC (0.0% vs. 16.7%, p=0.04). Conclusion: The utility of serum p53 Ab for detecting CAC is dubious in the era of immunosuppressive therapy.

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p53 expression in patients with ulcerative colitis - associated with dysplasia and carcinoma: a systematic meta-analysis

Cited by 22 publications

References 42 publications

<p>miR-370-3p Alleviates Ulcerative Colitis-Related Colorectal Cancer in Mice Through Inhibiting the Inflammatory Response and Epithelial-Mesenchymal Transition</p>

<p>miR-370-3p Alleviates Ulcerative Colitis-Related Colorectal Cancer in Mice Through Inhibiting the Inflammatory Response and Epithelial-Mesenchymal Transition</p>

Immunohistochemical Expression of CD133 and LGR5 in Ulcerative Colitis-associated Colorectal Cancer and Dysplasia

Uselessness of Serum p53 Antibody for Detecting Colitis-associated Cancer in the Era of Immunosuppressive Therapy

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