Multidrug resistance affects the prognosis of primary epithelial ovarian cancer

Gao, Bo; Yang, Fan; Chen, Wei; Li, Rui; Hu, Xiuxue; Liang, Yong; Li, Dongmin

doi:10.3892/ol.2019.10745

Cited by 11 publications

(9 citation statements)

References 34 publications

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“…Changes in glycosylation have been stated to cause the development of cancers. The modulation of the sialylation of different cell surface receptors promotes survival, proliferation, metastasis development and resistance to drugs and chemotherapy (7)(8)(9)(10). In addition to sialylation, aberrant fucosylation and a decrease in GlcNAcylation appear to play a role in solid cancer evolution (11,12).…”

Section: Introductionmentioning

confidence: 99%

Abnormal B cell glycosylation in autoimmunity: A new potential treatment strategy

Morel

Pochard²,

Echchih³

et al. 2022

Front. Immunol.

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Systemic lupus erythematosus (SLE) and primary Sjögren’s syndrome (pSS) are two autoimmune diseases characterised by the production of pathogenic autoreactive antibodies. Their aetiology is poorly understood. Nevertheless, they have been shown to involve several factors, such as infections and epigenetic mechanisms. They also likely involve a physiological process known as glycosylation. Both SLE T cell markers and pSS-associated autoantibodies exhibit abnormal glycosylation. Such dysregulation suggests that defective glycosylation may also occur in B cells, thereby modifying their behaviour and reactivity. This study aimed to investigate B cell subset glycosylation in SLE, pSS and healthy donors and to extend the glycan profile to serum proteins and immunoglobulins. We used optimised lectin-based tests to demonstrate specific glycosylation profiles on B cell subsets that were specifically altered in both diseases. Compared to the healthy donor B cells, the SLE B cells exhibited hypofucosylation, whereas only the pSS B cells exhibited hyposialylation. Additionally, the SLE B lymphocytes had more galactose linked to N-acetylglucosamine or N-acetylgalactosamine (Gal-GlcNAc/Gal-GalNAc) residues on their cell surface markers. Interestingly, some similar alterations were observed in serum proteins, including immunoglobulins. These findings indicate that any perturbation of the natural glycosylation process in B cells could result in the development of pathogenic autoantibodies. The B cell glycoprofile can be established as a preferred biomarker for characterising pathologies and adapted therapeutics can be used for patients if there is a correlation between the extent of these alterations and the severity of the autoimmune diseases.

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Section: Introductionmentioning

confidence: 99%

Abnormal B cell glycosylation in autoimmunity: A new potential treatment strategy

Morel

Pochard²,

Echchih³

et al. 2022

Front. Immunol.

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“…66,68 Analysis of patient samples has revealed RASSF1A methylation is more prominent in OC tissue than in benign tissue, with marked prevalence in chemoresistant OC samples. 69,70 Nevertheless, the extent of RASSF1A promoter hypermethylation across OC patients is less well-defined, the prevalence of this epimutation across OC cohorts has varied from 30% to almost 60%. 71,72 2.3 | Wnt/β-catenin signaling…”

Section: Rassf1amentioning

confidence: 99%

The role of DNA methylation in ovarian cancer chemoresistance: A narrative review

Song

Artibani

2023

Health Science Reports

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Background and Aims: Ovarian cancer (OC) is the most lethal gynecological cancer.In 2018, it was responsible for over 180,000 deaths worldwide. The high mortality rate is the culmination of a lack of early diagnosis and high rates of chemotherapy resistance, which is synonymous with disease recurrence. Over the last two decades, an increasingly significant role of epigenetic mechanisms, in particular DNA methylation, has emerged. This review will discuss several of the most significant genes whose hypo/hypermethylation profiles are associated with chemoresistance.Aside from functionally elucidating and evaluating these epimutations, this review will discuss recent trials of DNA methyltransferase inhibitors (DNMTi). Finally, we will propose future directions that could enhance the feasibility of utilizing these candidate epimutations as clinical biomarkers.Methods: To perform this review, a comprehensive literature search based on our keywords was conducted across the online databases PubMed and Google Scholar for identifying relevant studies published up until August 2022.Results: Epimutations affecting MLH1, MSH2, and Ras-association domain family 1 isoform A (DNA damage repair and apoptosis); ATP-binding cassette subfamily B member 1 and methylation-controlled J (drug export); secreted frizzled-related proteins (Wnt/β-catenin signaling), neurocalcin delta (calcium and G protein-coupled receptor signaling), and zinc finger protein 671 all have potential as biomarkers for chemoresistance. However, specific uncertainties relating to these epimutations include histotype-specific differences, intrinsic versus acquired chemoresistance, and the interplay with complete surgical debulking. DNMTi for chemoresistant OC patients has shown some promise; however, issues surrounding their efficacy and dose-limiting toxicities remain; a personalized approach is required to maximize their effectiveness. Conclusion:Establishing a panel of aberrantly methylated chemoresistance-related genes to predict chemoresponsiveness and patients' suitability to DNMTi could significantly reduce OC recurrence, while improving DNMTi therapy viability. To achieve this, a large-scale prospective genome-wide DNA methylation profile study

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“…This MDR is associated with the regulation and function of apoptotic pathways, intracellular pH, drug pumps, DNA damage repair ability, and drug detoxification. All of these mechanisms reduce the concentration of chemotherapeutic drugs inside the cell, and hyper-and hypomethylation of certain genes appear to play a role (121).…”

Section: Cancer Cells Present Therapy Resistance By Changing Their Dnmentioning

confidence: 99%

Role of DNA Methylation in the Resistance to Therapy in Solid Tumors

Romero-García¹,

Prado-Garcı́a²,

Carlos‐Reyes³

2020

Front. Oncol.

106

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Despite the recent advances in chemotherapeutic treatments against cancer, some types of highly aggressive and invasive cancer develop drug resistance against conventional therapies, which continues to be a major problem in the fight against cancer. In recent years, studies of alterations of DNA methylome have given us a better understanding of the role of DNA methylation in the development of tumors. DNA methylation (DNAm) is an epigenetic change that promotes the covalent transfer of methyl groups to DNA. This process suppresses gene expression through the modulation of the transcription machinery access to the chromatin or through the recruitment of methyl binding proteins. DNAm is regulated mainly by DNA methyltransferases. Aberrant DNAm contributes to tumor progression, metastasis, and resistance to current anti-tumoral therapies. Aberrant DNAm may occur through hypermethylation in the promoter regions of tumor suppressor genes, which leads to their silencing, while hypomethylation in the promoter regions of oncogenes can activate them. In this review, we discuss the impact of dysregulated methylation in certain genes, which impact signaling pathways associated with apoptosis avoidance, metastasis, and resistance to therapy. The analysis of methylome has revealed patterns of global methylation, which regulate important signaling pathways involved in therapy resistance in different cancer types, such as breast, colon, and lung cancer, among other solid tumors. This analysis has provided gene-expression signatures of methylated region-specific DNA that can be used to predict the treatment outcome in response to anti-cancer therapy. Additionally, changes in cancer methylome have been associated with the acquisition of drug resistance. We also review treatments with demethylating agents that, in combination with standard therapies, seem to be encouraging, as tumors that are in early stages can be successfully treated. On the other hand, tumors that are in advanced stages can be treated with these combination schemes, which could sensitize tumor cells that are resistant to the therapy. We propose that rational strategies, which combine specific demethylating agents with conventional treatment, may improve overall survival in cancer patients.

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Multidrug resistance affects the prognosis of primary epithelial ovarian cancer

Cited by 11 publications

References 34 publications

Abnormal B cell glycosylation in autoimmunity: A new potential treatment strategy

Abnormal B cell glycosylation in autoimmunity: A new potential treatment strategy

The role of DNA methylation in ovarian cancer chemoresistance: A narrative review

Role of DNA Methylation in the Resistance to Therapy in Solid Tumors

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