Expression and Mutation Pattern of β-Catenin and Adenomatous Polyposis Coli in Colorectal Cancer Patients

Abdelmaksoud-Damak, Rania; Miladi-Abdennadher, Imen; Triki, Mouna; Khabir, Abdelmajid; Charfi, Slim; Ayadi, Lobna; Frikha, M.; Sellami‐Boudawara, Tahya; Mokdad-Gargouri, Raja

doi:10.1016/j.arcmed.2015.01.001

Cited by 21 publications

(18 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[14,15,18–21,25–47] In addition, 9 studies showed a relationship between cytoplasmic β-catenin expression and pathological features or OS [17,19–21,25,33,34,37,43] (Table 2). Thirteen studies were selected for analysis of the prognostic value of reduced β-catenin expression in the membrane of CRC [17,19–21,26,31,34,35,38,43,48–50] (Table 3). There were also 3 studies included to examine the predictive role of nuclear β-catenin expression in the invasive front of tumor [17,41,51] (Table 4).…”

Section: Resultsmentioning

confidence: 99%

Nuclear expression and/or reduced membranous expression of β-catenin correlate with poor prognosis in colorectal carcinoma

et al. 2016

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 99%

Nuclear expression and/or reduced membranous expression of β-catenin correlate with poor prognosis in colorectal carcinoma

et al. 2016

View full text Add to dashboard Cite

show abstract

“…It has been found that the alterations of the β-catenin itself could also be responsible for elevated protein levels. Mutations in CTNNB1 gene, which substitute APC inactivation on a molecular level, have recently been described in colorectal carcinoma cell lines [21,43] as well as in colorectal cancer patients [31]. The mutations were found in exon 3 of the CTNNB1 gene and resulted in an amino acid change at GSK-3β phosphorylation sites at codons 33, 37, 41, and 45.…”

Section: Discussionmentioning

confidence: 99%

“…An association of β-catenin accumulation and malignancy has been shown for several tumor types, including colorectal carcinomas [21,31,32], hepatocellular carcinomas [12,33], endometroid ovarian carcinomas [34], melanomas [35], and desmoid tu- mors [36,37,38]. Although, the increased oncogenic β-catenin activity in these heterogeneous tumor types may be as a result of different mechanisms but colorectal carcinomas, desmoid tumors, and hepatoblastomas have in common that they more frequently affect patients with FAP (familial adenomatous polyposis).…”

Section: Discussionmentioning

confidence: 99%

β-Catenin accumulation and S33F mutation of CTNNB1 gene in colorectal cancer in Saudi Arabia

Alomar¹,

Mansour

Abuderman³

et al. 2016

pjp

View full text Add to dashboard Cite

Several risk factors associated with colorectal cancer (CRC) have been identified including β-catenin/CTNNB1 hotspot mutations. The levels of β-catenin within a cell are regulated via phosphorylation of the N terminus of β-catenin by GSK-3β. Thus far three serines (S33, 37, 45) and one threonine (T41) are considered to be the substrates for GSK-3β phosphorylation. In the present investigation an attempt was made to study the role of β-catenin mutations in exon-3 in 60 colorectal cancer patients from Kingdom of Saudi Arabia (KSA). The hot spot mutation region of β-catenin exon 3 was evaluated in matched tumor and normal tissues using PCR and direct sequencing. Sequencing of exon 3 of the CTNNB1 gene revealed an activating mutation (S33F) in one of the tumor samples as compared to the normal tissue from the same patient where there was no such mutation found. Immunohistochemical staining showed the accumulation of β-catenin protein both in cytoplasm and in the nuclei of cancer cells as compared to normal tissue.

show abstract

“…Therefore, Wnt-signalling may be switched into the ON-state even in the absence of Wnt ligand–receptor interaction, leading to the characteristic sequence of ON-state activity: disassembly of the destruction complex, loss of phosphorylation and degradation of β-catenin and activation of Wnt-induced gene transcription, which all contributes to cancer progression. Mutations in CTNNB1 , the gene for β-catenin, have been implicated in colon cancer, gastric cancer, medulloblastoma, melanoma, ovarian cancer, pancreatic cancer, and prostate cancer [41, 42]. Mutations in APC gene have frequently been identified in colon cancer as well, while mutations in AXIN1 , the gene for Axin1, have been identified in hepatocellular carcinoma [43] and medulloblastoma [44].…”

Section: Main Textmentioning

confidence: 99%

Wnt-signalling pathways and microRNAs network in carcinogenesis: experimental and bioinformatics approaches

2016

View full text Add to dashboard Cite

Over the past few years, microRNAs (miRNAs) have not only emerged as integral regulators of gene expression at the post-transcriptional level but also respond to signalling molecules to affect cell function(s). miRNAs crosstalk with a variety of the key cellular signalling networks such as Wnt, transforming growth factor-β and Notch, control stem cell activity in maintaining tissue homeostasis, while if dysregulated contributes to the initiation and progression of cancer. Herein, we overview the molecular mechanism(s) underlying the crosstalk between Wntsignalling components (canonical and non-canonical) and miRNAs, as well as changes in the miRNA/Wnt-signalling components observed in the different forms of cancer. Furthermore, the fundamental understanding of miRNAmediated regulation of Wnt-signalling pathway and vice versa has been significantly improved by high-throughput genomics and bioinformatics technologies. Whilst, these approaches have identified a number of specific miRNA(s) that function as oncogenes or tumour suppressors, additional analyses will be necessary to fully unravel the links among conserved cellular signalling pathways and miRNAs and their potential associated components in cancer, thereby creating therapeutic avenues against tumours. Hence, we also discuss the current challenges associated with Wnt-signalling/miRNAs complex and the analysis using the biomedical experimental and bioinformatics approaches.

show abstract

Expression and Mutation Pattern of β-Catenin and Adenomatous Polyposis Coli in Colorectal Cancer Patients

Cited by 21 publications

References 46 publications

Nuclear expression and/or reduced membranous expression of β-catenin correlate with poor prognosis in colorectal carcinoma

Nuclear expression and/or reduced membranous expression of β-catenin correlate with poor prognosis in colorectal carcinoma

β-Catenin accumulation and S33F mutation of CTNNB1 gene in colorectal cancer in Saudi Arabia

Wnt-signalling pathways and microRNAs network in carcinogenesis: experimental and bioinformatics approaches

Contact Info

Product

Resources

About