MicroRNA 153-1 (miR-153-1)

MicroRNA 153-1 (miR-153-1) is a non-coding RNA molecule classified as a microRNA that regulates gene expression post-transcriptionally by binding to complementary sequences in target mRNAs, leading to their degradation or inhibition of translation[5][3]. miR-153-1 (including its mature forms miR-153-5p and miR-153-3p) plays key roles in cancer biology, acting as both a tumor suppressor and, in some contexts, as an oncogene, by targeting genes involved in cell proliferation, apoptosis, invasion, and EMT in a variety of cancers including renal cell carcinoma and gastric cancer[1][2][3]. It is also implicated in neurobiology, especially in the survival of cortical neurons and the pathophysiology of neurodegenerative diseases such as Alzheimer’s disease, through regulation of genes like APP and SNCA[4][6]. Its expression level can serve as a prognostic or diagnostic biomarker in certain cancers, but its dual, context-dependent roles pose therapeutic challenges[3]. miR-153-1 is annotated in GeneCards as a microRNA-class gene associated with renal cell carcinoma[5]. miR-153-1 can suppress or promote cancer, depending on the cellular context and gene targets (e.g., suppresses KLF5 in gastric cancer, but targets AGO1 in renal carcinoma)[1][2][3]. In Alzheimer’s disease, miR-153-1 targets genes such as APP, SORL1, PICALM, and PSEN1, all involved in AD pathogenesis, and regulation of amyloid processing and synapse formation[4][6]. miR-153-1 does not directly interact with drugs as a protein target would; modulation is generally achieved using miRNA mimics or inhibitors, but clinical drugs specifically targeting miR-153-1 are not yet listed[3]. Safety concerns stem from its context-dependent dual roles in cancer progression, making therapeutic targeting complex and highly specific to tissue or disease state[3].

Other names

hsa-mir-153-1MIRN153-1mir-153-1MIR153-1miR-153miR-153-5pmiR-153-3p

Regulation of mRNA stability and translation via binding to target transcripts. Downregulation of oncogenes (e.g., Bcl-2, Mcl-1, XIAP). Regulation of tumor suppressor genes (e.g., PTEN, AGO1). Modulation of signaling pathways (e.g., PI3K/Akt pathway).