MicroRNA-148a (miR-148a) (miR-148a)

MicroRNA-148a (miR-148a) is a small non-coding RNA molecule that functions as a critical post-transcriptional regulator of gene expression by binding to the 3' untranslated regions (UTRs) of specific messenger RNAs (mRNAs) [1]. It is involved in a wide array of biological processes, including cell proliferation, apoptosis, and the regulation of lipid metabolism, particularly through its influence on the low-density lipoprotein receptor (LDLR) [2]. In oncology, miR-148a often acts as a tumor suppressor, and its downregulation is associated with the progression of gastric, colorectal, and liver cancers [3]. Conversely, its overexpression has been linked to certain autoimmune conditions like systemic lupus erythematosus and metabolic dysregulation [4]. Therapeutic strategies currently under investigation include the use of miRNA mimics to restore its suppressive activity in cancer or antisense oligonucleotides (antagomirs) to inhibit its action in metabolic and inflammatory diseases [5]. The primary challenges in developing miR-148a-targeted therapies involve ensuring stable delivery to target tissues and minimizing off-target effects resulting from the broad regulatory network of this miRNA [6]. Citations: [1] miRBase: The microRNA database. [2] Goedeke, L., et al. (2015). "MicroRNA-148a regulates LDL receptor and ABCA1 expression to control circulating lipoprotein levels." Nature Medicine. [3] Li, Y., et al. (2016). "MicroRNA-148a: a tumor suppressor or an oncogene?" Oncotarget. [4] Pan, W., et al. (2010). "MicroRNA-148a contributes to the pathogenesis of systemic lupus erythematosus." Annals of the Rheumatic Diseases. [5] Rupaimoole, R., & Slack, F. J. (2017). "MicroRNA therapeutics: towards a new era for the management of cancer and other diseases." Nature Reviews Drug Discovery. [6] Wang, J., et al. (2018). "The role of MicroRNA-148a in cancer." Journal of Cancer.

Other names

MIR148Ahsa-miR-148amicroRNA 148amiR-148a-3pmiR-148a-5p

miRNA mimics function by replenishing deficient miR-148a levels to suppress target oncogenes, while antagomirs act as competitive inhibitors that bind to miR-148a, preventing it from silencing target mRNAs such as LDLR or ABCA1.