Aberrant Promoter Hypermethylation of p16 and RASSF1a Genes in Colorectal Cancer – Significance in Young Patients

Sugara, Medha; Ramachandra, C.; Kumar, K.V. Veerendra; Ramesh, Gayathri; Swamy, Shalini N; Kumar, Sandeep

doi:10.1007/s13193-021-01325-5

Cited by 3 publications

(1 citation statement)

References 24 publications

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“…In 2000, Dammann et al, first reported that the loss of expression of RASSF1A in lung cancer was associated with methylation of its CpG-island promoter [ 59 ]. Numerous research studies have demonstrated the abnormal expression of RASSF1A in different kinds of tumors, such as nasopharyngeal carcinoma, breast cancers, and ECs [ 60 , 61 , 62 ]. The overwhelming majority of reports revealed that the CpG island in the RASSF1A promoter was hypermethylated, which has been linked to the malignant transition of early benign tumors into later invasive carcinomas [ 63 , 64 ].…”

Section: Tumor Suppressor Genesmentioning

confidence: 99%

Research Progress of DNA Methylation in Endometrial Cancer

Ding

Chen

et al. 2022

Biomolecules

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Endometrial cancer (EC)) is one of the most common malignant tumors of the female genital system, with an increasing incidence and mortality, worldwide. Although the therapeutic strategy of EC is still complicated and challenging, further understanding of carcinogenesis from a gene perspective would allow an effort to improve therapeutic precision in this complex malignancy. DNA methylation is the most widely studied epigenetic alteration in human tumors. Aberrant DNA methylation events, resulting in altered gene expression, are features of many tumor types. In this review, we provide an update on evidence about the roles of aberrant DNA methylation within some classical tumor suppressor genes and oncogenes in endometrial carcinogenesis, and report on recent advances in the understanding of the contribution of aberrant DNA methylation to EC, as well as opportunities and challenges of DNA methylation in EC management and prevention.

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Section: Tumor Suppressor Genesmentioning

confidence: 99%

Research Progress of DNA Methylation in Endometrial Cancer

Ding

Chen

et al. 2022

Biomolecules

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Therapeutic targeting of DNA methylation alterations in cancer

Lee,

Nestler,

Chiappinelli

2024

Pharmacology & Therapeutics

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The up-regulation of SYNCRIP promotes the proliferation and tumorigenesis via DNMT3A/p16 in colorectal cancer

Li,

Lu,

Chen

et al. 2024

Sci Rep

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Heterogeneous nuclear ribonucleoproteins (hnRNPs), a group of proteins that control gene expression, have been implicated in many post-transcriptional processes. SYNCRIP (also known as hnRNP Q), a subtype of hnRNPs, has been reported to be involved in mRNA splicing and translation. In addition, the deregulation of SYNCRIP was found in colorectal cancer (CRC). However, the role of SYNCRIP in regulating CRC growth remains largely unknown. Here, we found that SYNCRIP was highly expressed in colorectal cancer by analyzing TCGA and GEPIA database. Furthermore, we confirmed the expression of SYNCRIP expression in CRC tumor and CRC cell lines. Functionally, SYNCRIP depletion using shRNA in CRC cell lines (SW480 and HCT 116) resulted in increased caspase3/7 activity and decreased cell proliferation, as well as migration. Meanwhile, overexpression of SYNCRIP showed opposite results. Mechanistically, SYNCRIP regulated the expression of DNA methyltransferases (DNMT) 3A, but not DNMT1 or DNMT3B, which affected the expression of tumor suppressor, p16. More importantly, our in vivo experiments showed that SYNCRIP depletion significantly inhibited colorectal tumor growth. Taken all together, our results suggest SYNCRIP as a potent therapeutic target in colorectal cancer.

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Aberrant Promoter Hypermethylation of p16 and RASSF1a Genes in Colorectal Cancer – Significance in Young Patients

Cited by 3 publications

References 24 publications

Research Progress of DNA Methylation in Endometrial Cancer

Research Progress of DNA Methylation in Endometrial Cancer

Therapeutic targeting of DNA methylation alterations in cancer

The up-regulation of SYNCRIP promotes the proliferation and tumorigenesis via DNMT3A/p16 in colorectal cancer

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