Senescence-induced long noncoding RNA (sin-lncRNA)

Senescence-induced long noncoding RNA (sin-lncRNA), also named RIPOR3 antisense RNA 1 (RIPOR3-AS1), is an intronic lncRNA located on human chromosome 20, transcribed antisense to the protein-coding gene RIPOR3[1]. Sin-lncRNA is specifically and strongly induced in cellular senescence, including contexts such as replicative, oncogene-induced, and therapy-induced (e.g., cisplatin treatment in ovarian cancer cells) senescence[1]. Its function is to maintain metabolic homeostasis in non-proliferating senescent cells through regulation of mitochondrial metabolism, particularly by interacting with the enzyme dihydrolipoamide S-succinyltransferase (DLST), aiding retention of this enzyme in mitochondria and sustaining oxidative phosphorylation[1]. Loss or depletion of sin-lncRNA leads to DLST nuclear translocation, reduction in oxidative phosphorylation gene expression, increased metabolic dysfunction, and heightened oxidative stress, reinforcing the senescence phenotype[1]. Sin-lncRNA is regulated by the C/EBPβ transcription factor and acts as a senescence-specific regulator, contributing to metabolic rewiring and the control of stress responses in aging cells[1][4]. Depletion of sin-lncRNA in senescent cancer cells increases sensitivity to chemotherapeutics like cisplatin[1]. No direct drugs are known to specifically target this RNA, and it is not a classical "therapeutic target" such as a receptor, enzyme, or transporter, but its involvement in senescence and therapy resistance makes it a candidate for future research in anti-cancer strategies[1].

Other names

RIPOR3 antisense RNA 1RIPOR3-AS1senescence-induced lncRNAsin-lncRNA

Not direct drug targeting; sin-lncRNA expression is induced in senescence (e.g., by chemotherapy like cisplatin), and its depletion sensitizes cells to treatment by promoting metabolic dysfunction and oxidative stress[1].