Study of p53 and bcl-2 Oncoproteins in Ulcerative Colitis with Dysplasia

Kinra, Prateek; Turlapati, Spv; Mehta, Anurag; Rai, Ramji

doi:10.1016/s0377-1237(05)80006-1

Cited by 6 publications

(3 citation statements)

References 15 publications

(18 reference statements)

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“…Colorectal carcinoma arising on the ground of UC is, commonly, the result of a multistep process including inflamed mucosa without dysplasia, then low-grade dysplasia, high-grade dysplasia, and finally invasive adenocarcinoma, although each of the premalignant lesions can evolve directly towards carcinoma, without the intermediate steps [ 19 , 20 ].…”

Section: Introductionmentioning

confidence: 99%

Expression Profile of p53 and p21 in Large Bowel Mucosa as Biomarkers of Inflammatory-Related Carcinogenesis in Ulcerative Colitis

et al. 2016

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Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease that slightly increases the risk of colorectal cancer in patients with long-standing extended disease. Overexpression of p53 and p21 in colonic epithelia is usually detected in UC patients when no dysplasia is histologically seen and it is used by pathologists as a discriminator between regenerative changes and intraepithelial neoplasia, as well as a tissue biomarker useful to predict the risk of evolution toward malignancy. We present a one-year prospective observational study including a cohort of 45 patients with UC; p53 and p21 were evaluated in epithelial cells. p53 was positive in 74 samples revealed in 5% to 90% of epithelial cells, while 63 biopsies had strong positivity for p21 in 5% to 50% of epithelial cells. Architectural distortion was significantly correlated with p53 overexpression in epithelial cells. Thus, we consider that architectural distortion is a good substitute for p53 and p21 expression. We recommend use of p53 as the most valuable tissue biomarker in surveillance of UC patients, identifying the patients with higher risk for dysplasia. Association of p21 is also recommended for a better quantification of risk and for diminishing the false-negative results.

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Section: Introductionmentioning

confidence: 99%

Expression Profile of p53 and p21 in Large Bowel Mucosa as Biomarkers of Inflammatory-Related Carcinogenesis in Ulcerative Colitis

et al. 2016

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“…BCL2, a prototype gene in the BCL family, exhibits anti‐apoptotic activity and is located in the outer leaflet of mitochondria. BCL2 regulates antioxidant pathways, thereby protecting cells from apoptosis 42 . We also examined the expression of BAX, which is known to accelerate apoptosis.…”

Section: Discussionmentioning

confidence: 99%

“…BCL2 regulates antioxidant pathways, thereby protecting cells from apoptosis. 42 We also examined the expression of BAX, which is known to accelerate apoptosis. Under stress conditions, BAX is conformationally modified and translocated to the mitochondrial membrane, accompanied by the subsequent release of cytochrome C, triggering caspase-3.…”

Section: Mip-1α Can Boost Local T-cell Responses By Enhancing the Mov...mentioning

confidence: 99%

The therapeutic effects of cycloastragenol in ulcerative colitis by modulating SphK/MIP‐1α/miR‐143 signalling

Bagalagel

Diri

Noor

et al. 2022

Basic Clin Pharma Tox

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Patients with ulcerative colitis (UC) experience diarrhoea, hematochezia and abdominal pain. UC is a well-known health challenge affecting 200-250 per 100 000 individuals worldwide, with a similar prevalence in both sexes and elevated upon activation of gut immune responses. We evaluated the potential therapeutic effects of cycloastragenol in experimentally induced UC rats and examined the modulation of sphingosine kinase (SphK), macrophage inflammatory protein (MIP)-1α and miR-143. We treated UC rats with 30 mg/kg cycloastragenol and assessed gene and protein expression levels of SphK, MIP-1α, B-cell lymphoma 2 (BCL2), BCL2-associated X (BAX), miR-143, NF-κB, tumour necrosis factor (TNF)-α and active caspase-3. Colon sections were examined using electron microscopy; additional sections were stained with haematoxylin-eosin or immunostained with anti-TNF-α and anti-caspase-3 antibodies. Electron microscopy of UC specimens revealed dark distorted goblet cell nuclei with disarranged mucus granules and a nondistinct brush border with atypical microvilli. Haematoxylin-eosin staining showed damaged intestinal glands, severe haemorrhage and inflammatory cell infiltration. Cycloastragenol treatment improved the induced morphological changes. In UC rats, cycloastragenol significantly reduced expression levels of SphK, MIP-1α, BAX, NF-κB, TNF-α and active caspase-3, associated with BCL2 and miR-143 overexpression. Therefore, cycloastragenol protects against UC by modulating SphK/MIP-1α/miR-143, subsequently deactivating inflammatory and apoptotic pathways.K E Y W O R D S active caspase-3, B-cell lymphoma 2 (BCL2), BCL2 associated X (BAX), macrophage inflammatory protein (MIP)-1α, miR-143, nuclear factor (NF)κB, sphingosine kinase (SphK), tumour necrosis factor (TNF)-α

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Therapeutic effects of genistein in experimentally induced ulcerative colitis in rats via affecting mitochondrial biogenesis

et al. 2023

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Study of p53 and bcl-2 Oncoproteins in Ulcerative Colitis with Dysplasia

Cited by 6 publications

References 15 publications

Expression Profile of p53 and p21 in Large Bowel Mucosa as Biomarkers of Inflammatory-Related Carcinogenesis in Ulcerative Colitis

Expression Profile of p53 and p21 in Large Bowel Mucosa as Biomarkers of Inflammatory-Related Carcinogenesis in Ulcerative Colitis

The therapeutic effects of cycloastragenol in ulcerative colitis by modulating SphK/MIP‐1α/miR‐143 signalling

Therapeutic effects of genistein in experimentally induced ulcerative colitis in rats via affecting mitochondrial biogenesis

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