MicroRNA 4717 (miR-4717)

MicroRNA 4717 (miR-4717) is a small, non-coding RNA molecule that regulates gene expression post-transcriptionally by binding to target mRNA 3'UTRs, leading to degradation or translational repression. It is involved in diverse physiological and pathological processes: - In hepatitis B virus (HBV) infection, miR-4717 regulates the expression of the immune checkpoint receptor PD-1 in an allele-specific manner, influencing immune responses and disease progression[1][2]. - In colorectal cancer, miR-4717 is upregulated—particularly following Fusobacterium nucleatum infection—where it promotes tumor cell proliferation by targeting and suppressing the tumor suppressor MAP2K4 and CREBBP[3][4]. - Its levels and activities reflect and potentially drive pathology, making it both a candidate diagnostic/prognostic biomarker and a potential (albeit challenging) target for therapeutic intervention. There are no currently approved drugs that directly target miR-4717, but miRNA mimics and inhibitors provide a proof-of-principle in experimental systems. Extreme caution is warranted in therapeutic approaches, given its complex roles in cancer and immune regulation[1][2][3][4].

Other names

hsa-mir-4717microRNA-4717miRNA-4717miR-4717-3p

Post-transcriptional gene silencing through direct binding to 3' untranslated regions (UTRs) of target mRNAs (e.g., PD-1[1][2], MAP2K4[3], CREBBP[4]), leading to mRNA degradation or translational repression. Immune modulation by allele-specific regulation of PD-1 expression, affecting T cell cytokine production (TNF-α, IFN-γ) and potentially altering susceptibility to disease and immune-mediated pathogenesis[1][2]. Promotion of cancer cell proliferation by suppressing tumor suppressor genes such as MAP2K4 and CREBBP, especially in the context of colorectal cancer and Fusobacterium nucleatum infection[3][4].