Mismatch repair gene expression in gastroesophageal cancers

Dracea, Amelia; Angelescu, C; Dănciulescu, Mihaela; Ciurea, Marius Eugen; Ioana, Mihai; Burada, Florin

doi:10.5152/tjg.2015.0139

Cited by 3 publications

(3 citation statements)

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“…Previous studies have found a clear correlation between ASF1B expression and immune cell infiltration, affecting tumor progression by altering immune infiltration. [ 23 ] It is suggested that ASF1B may promote cancer cell proliferation by altering the immune microenvironment of STAD. In addition, we found that TMB and MSI were positively correlated with ASF1B expression, with the high ASF1B expression group showing higher tumor heterogeneity, which was generally associated with impaired immunity and poorer survival.…”

Section: Discussionmentioning

confidence: 99%

ASF1B acted as a prognostic biomarker for stomach adenocarcinoma

Zhao,

Zhou,

Xing

et al. 2023

Medicine

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Stomach adenocarcinoma (STAD) has a high mortality rate due to the lack of highly sensitive biomarkers. Therefore, the search for potential tumor markers is of great value. ASF1B is a prognostic marker for a variety of tumors, while the prognostic value and immune microenvironment of ASF1B in STAD remain unclear, and to be determined. Kaplan–Meier analysis was performed to analyze the prognostic role of ASF1B in STAD. Functional enrichment of ASF1B was explored with GO and KEGG pathway analysis. We also explored the correlation between ASF1B expression and immune infiltration in STAD. ASF1B was significantly upregulated in STAD tissues and high expression of ASF1B indicated a poor overall survival, progression-free survival, and first progression rate in STAD. The functional enrichment analysis of ASF1B and related genes showed high enrichment in the cell cycle and DNA repair, and the ASF1B high expression group was also mainly enriched in pathways such as the cell cycle. Analysis of tumor immune infiltration showed that ASF1B expression was significantly associated with the majority of immune cell infiltration in STAD. Moreover, STAD patients with high ASF1B expression had a higher tumor mutation burden score, microsatellite instability score, PD-1 immunophenoscore, and immune checkpoint expression. Our results suggest that ASF1B was an independent prognostic factor for STAD as well as a potential target for immunotherapy.

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Section: Discussionmentioning

confidence: 99%

ASF1B acted as a prognostic biomarker for stomach adenocarcinoma

Zhao,

Zhou,

Xing

et al. 2023

Medicine

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“…These findings are in accordance with other studies showing increased expression of MSH2 in cancers such as gastric cancer. 79,80 The increased expression of MSH2 in fibroid tumors as compared to adjacent myometrium samples may be due to several possible mechanisms. It is possible that increased expression of MSH2 could be a cellular adaption for DNA lesion repair.…”

Section: Discussionmentioning

confidence: 99%

“…Another explanation may be that the increased expression of MSH2 could represent a possible response to the rapidly growing number of replication errors in the fibroid tissue with an increased rate of cell divisions. 79,80 Moreover, MSH2 levels can be reduced by ubiquitin-proteasome pathway. 81 Since PRC has been shown to regulate several DNA repair genes, we performed experiment to determine whether EZH2 regulates MSH2 expression.…”

Section: Discussionmentioning

confidence: 99%

Identification of Polycomb Group Protein EZH2-Mediated DNA Mismatch Repair Gene MSH2 in Human Uterine Fibroids

et al. 2016

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Uterine fibroids (UFs) are benign smooth muscle neoplasms affecting up to 70% of reproductive age women. Treatment of symptomatic UFs places a significant economic burden on the US health-care system. Several specific genetic abnormalities have been described as etiologic factors of UFs, suggesting that a low DNA damage repair capacity may be involved in the formation of UF. In this study, we used human fibroid and adjacent myometrial tissues, as well as an in vitro cell culture model, to evaluate the expression of MutS homolog 2 (MSH2), which encodes a protein belongs to the mismatch repair system. In addition, we deciphered the mechanism by which polycomb repressive complex 2 protein, EZH2, deregulates MSH2 in UFs. The RNA expression analysis demonstrated the deregulation of MSH2 expression in UF tissues in comparison to its adjacent myometrium. Notably, protein levels of MSH2 were upregulated in 90% of fibroid tissues (9 of 10) as compared to matched adjacent myometrial tissues. Human fibroid primary cells treated with 3-deazaneplanocin A (DZNep), chemical inhibitor of EZH2, exhibited a significant increase in MSH2 expression (P < .05). Overexpression of EZH2 using an adenoviral vector approach significantly downregulated the expression of MSH2 (P < .05). Chromatin immunoprecipitation assay demonstrated that enrichment of H3K27me3 in promoter regions of MSH2 was significantly decreased in DZNep-treated fibroid cells as compared to vehicle control. These data suggest that EZH2-H3K27me3 regulatory mechanism dynamically changes the expression levels of DNA mismatch repair gene MSH2, through epigenetic mark H3K27me3. MSH2 may be considered as a marker for early detection of UFs.

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