Noc2l, also known as Nir, is a nucleolar associated transcriptional repressor and a novel inhibitor of histone acetyltransferase (INHAT) [1]. It has two INHAT function domains and regulates histone acetylation in a histone deacetylases (HDAC) independent manner. Noc2l is involved in multiple biological processes such as P53-mediated transcription, ribosome RNA processing, certain development events and carcinogenesis [1].

In cervical cancer, lncRNA NOC2L-4.1 functions as a tumor oncogene by regulating the miR-630/YAP1 pathway. Downregulation of lncRNA NOC2L-4.1 suppresses cervical cancer cell migration and proliferation [2]. In ovarian cancer, NOC2L promotes paclitaxel resistance by decreasing NDUFA4 through histone acetylation suppression, remodeling energy metabolism towards aerobic glycolysis [3]. In preeclampsia, NOC2L is downregulated in placental tissues. Overexpression of NOC2L increases cell proliferation and inhibits apoptosis in placental trophoblast cells [4]. Genome-wide meta-analysis identified rs13303010 at 1p36.33 (NOC2L) as a new susceptibility locus for pancreatic cancer [5]. In the epidermis, Nir (Noc2l) deficiency impairs epidermal stratification and barrier function, inhibits cell proliferation, and increases apoptosis and p53 acetylation [6]. Bioinformatic analyses suggest that NOC2L may have dual roles in tumorigenesis, with overexpression promoting tumor growth and reduced expression exerting tumor-suppressive effects [7].

In conclusion, Noc2l is involved in diverse biological functions, particularly in histone acetylation regulation, and has significant implications in various diseases including cancers and preeclampsia. Studies using in vivo models like those in cancer and preeclampsia research have helped to uncover its role in disease-related biological processes, providing potential targets for biomarker discovery and therapeutic intervention.