Molecular epigenetic dynamics in breast carcinogenesis

Hazra, Aadrita; Bose, Pritha; Sunita, Priyashree; Pattanayak, Shakti Prasad

doi:10.1007/s12272-021-01348-0

Cited by 14 publications

(9 citation statements)

References 147 publications

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“…The methylation of DNA and histones drives cell division and regulation of gene expression through epigenesis and imprinting [35]. Thus, folate de ciency could affect the stability of DNA and increase the risk of malignancy through either altered DNA methylation that may lead to proto-oncogenes activation or by alteration of DNA synthesis and DNA repair [36].…”

Section: Discussionmentioning

confidence: 99%

Associations of Methylenetetrahydrofolate reductase (MTHFR) polymorphism with Hepatocellular carcinoma In Egyptian population.

Abozeid,

zaki,

nagah

et al. 2023

Preprint

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Liver serves as a hub for key metabolic pathways such as folate cycle that provides one-carbon units for a network of metabolic reactions. Methylenetetrahydrofolate reductase (MTHFR) is a rate limiting enzyme in folate metabolism and thus it is vital for DNA methylation, synthesis and repair. The objective of this study was to evaluate an eventual association between MTHFR polymorphisms C677T (rs1801133) and A1298C (rs1801131) and the susceptibility to hepatocellular carcinoma (HCC) in Egyptian population. Blood samples from patients and controls from Mansoura university hospital were used after signed consent and approvement from Medical ethical committee. The two genetic loci were designed for amplification and genotyped by using PCR-RFLP. Our results clarify that, the most important predictors for HCC are T/T genotype of variant C677T and C/C genotype of variant (A1298C) with odds ratio 39.756, and 2.012 respectively. Also, MTHFR variant C677T genotype C/C or T/T combined with MTHFR variant A1298C genotype C/C were associated with an increased risk of HCC, with the OR, 2.6 and 7 respectively. CT genotype of MTHFR variant C677T showed significant difference between HCC grades and C allele of variant C677T showed significant difference in BCLC stages of HCC. Our data indicates that, the two variants (C677T and A1298C) constitute a risk factor for the development of HCC and this could be attributed to the low activities of the enzyme MTHFR that disturb one carbon metabolism and subsequently, DNA synthesis, repair and Methylation, cellular redox state, growth, and proliferation.

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Section: Discussionmentioning

confidence: 99%

Associations of Methylenetetrahydrofolate reductase (MTHFR) polymorphism with Hepatocellular carcinoma In Egyptian population.

Abozeid,

zaki,

nagah

et al. 2023

Preprint

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“…Generally, DNA hypermethylation inhibits gene expression while DNA hypomethylation activates gene expression. Aberrant DNA methylation directly or indirectly alters the transcription of tumor suppressors and carcinogenesis factors, thereby accelerating the development of BC [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Crosstalk between Methylation and ncRNAs in Breast Cancer: Therapeutic and Diagnostic Implications

Liu

Leng

Liu

et al. 2022

IJMS

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Breast cancer, as a highly heterogeneous malignant tumor, is one of the primary causes of death among females worldwide. The etiology of breast cancer involves aberrant epigenetic mechanisms and abnormal expression of certain non-coding RNA (ncRNAs). DNA methylation, N6-methyladenosine(m6A), and histone methylation are widely explored epigenetic regulation types in breast cancer. ncRNAs are a group of unique RNA transcripts, mainly including microRNA (miRNAs), long non-coding RNA (lncRNAs), circular RNA (circRNAs), small interfering RNA (siRNAs), piwi-interacting RNA (piRNAs), etc. Different types of methylation and ncRNAs mutually regulate and interact to form intricate networks to mediate precisely breast cancer genesis. In this review, we elaborate on the crosstalk between major methylation modifications and ncRNAs and discuss the role of their interaction in promoting breast cancer oncogenesis. This review can provide novel insights into establishing a new diagnostic marker system on methylation patterns of ncRNAs and therapeutic perspectives of combining ncRNA oligonucleotides and phytochemical drugs for breast cancer therapy.

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“…This renders the APC unable to bind to Axin or degrade β-catenin [9], resulting in the aberrant activation of Wnt signaling and the continuous expression of Wnt target genes. The mammalian target of rapamycin (mTOR) is a key regulator of various intracellular and extracellular signaling processes [10][11][12]. The most significant downstream effector, ribosomal protein S6 kinase 1 (S6K1), is known to play a critical role in nucleotide and protein synthesis, which is essential for cell growth and proliferation [13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Nuclear S6K1 Enhances Oncogenic Wnt Signaling by Inducing Wnt/β-Catenin Transcriptional Complex Formation

Lee

Park

et al. 2022

IJMS

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Ribosomal protein S6 kinase 1 (S6K1), a key downstream effector of the mammalian target of rapamycin (mTOR), regulates diverse functions, such as cell proliferation, cell growth, and protein synthesis. Because S6K1 was previously known to be localized in the cytoplasm, its function has been mainly studied in the cytoplasm. However, the nuclear localization and function of S6K1 have recently been elucidated and other nuclear functions are expected to exist but remain elusive. Here, we show a novel nuclear role of S6K1 in regulating the expression of the Wnt target genes. Upon activation of the Wnt signaling, S6K1 translocated from the cytosol into the nucleus and subsequently bound to β-catenin and the cofactors of the Wnt/β-catenin transcriptional complex, leading to the upregulation of the Wnt target genes. The depletion or repression of S6K1 downregulated the Wnt target gene expression by inhibiting the formation of the Wnt/β-catenin transcriptional complex. The S6K1-depleted colon cancer cell lines showed lower transcription levels of the Wnt/β-catenin target genes and a decrease in the cell proliferation and invasion compared to the control cell lines. Taken together, these results indicate that nuclear S6K1 positively regulates the expression of the Wnt target genes by inducing the reciprocal interaction of the subunits of the transcriptional complex.

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Molecular epigenetic dynamics in breast carcinogenesis

Cited by 14 publications

References 147 publications

Associations of Methylenetetrahydrofolate reductase (MTHFR) polymorphism with Hepatocellular carcinoma In Egyptian population.

Associations of Methylenetetrahydrofolate reductase (MTHFR) polymorphism with Hepatocellular carcinoma In Egyptian population.

Crosstalk between Methylation and ncRNAs in Breast Cancer: Therapeutic and Diagnostic Implications

Nuclear S6K1 Enhances Oncogenic Wnt Signaling by Inducing Wnt/β-Catenin Transcriptional Complex Formation

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