Cytidine residues in nucleic acids (C)

Cytidine residues are essential pyrimidine nucleosides that serve as fundamental building blocks of both DNA and RNA, playing a central role in the storage and transmission of genetic information [1]. In the context of epigenetics, cytidine residues in DNA are the primary sites for methylation by DNA methyltransferases (DNMTs) to form 5-methylcytosine, a modification critical for gene silencing, genomic stability, and cellular differentiation [2]. Abnormal methylation patterns, particularly hypermethylation of tumor suppressor gene promoters, are a hallmark of various malignancies, including leukemia and solid tumors [4]. Therapeutic intervention often involves cytidine analogs like azacitidine and decitabine, which mimic natural cytidine and are incorporated into the genome of cancer cells [3]. These agents function by trapping DNMT enzymes or disrupting nucleic acid synthesis, thereby reversing pathogenic epigenetic states or inducing cytotoxic effects in malignant cell populations [3,4].

Other names

Cytosine2'-DeoxycytidineRibocytidine5-MethylcytosinedCrC

Drugs targeting cytidine residues typically act as nucleoside analogs that are incorporated into DNA or RNA during synthesis. Once incorporated, they can covalently bind and inhibit DNA methyltransferases (DNMTs), leading to global DNA hypomethylation and the reactivation of silenced tumor suppressor genes. Additionally, some analogs act as antimetabolites by causing DNA chain termination or inducing DNA damage and apoptosis in rapidly dividing cells.