miR-17: from developmental regulatory hub to molecular engine driving tumourigenesis

MicroRNA-17(miR-17) is a prototypical oncogenic miRNA that plays a central driving role in the initiation and progression of various malignant tumours (MT), including lymphoma, lung cancer, colorectal cancer (CRC), and breast cancer (BC). It inhibits the activation of apoptosis pathways and promotes the G1/S phase transition by targeting tumor suppressor genes and cell cycle regulators, thereby driving the unlimited proliferation of tumor cells. Concurrently, it targets molecules associated with epithelial-mesenchymal transition (EMT), activating key signalling pathways, such as Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/AKT) and Wnt/Beta-catenin(Wnt/β-catenin) to enhance the invasiveness and migration capabilities of tumour cells. Moreover, miR-17 participates in a cross-regulatory network of non- coding RNAs(ncRNAs), acting both as a molecular sponge to sequester long non-coding RNAs(lncRNAs) and circular RNAs(circRNAs), and as a regulator of the stability or biogenesis of these ncRNAs.This further amplifies oncogenic effects, induces tumor cell resistance to chemotherapy and radiotherapy, and ultimately synergistically promotes tumor angiogenesis, thereby remodeling the tumor microenvironment(TME). In clinical applications, miR-17 holds potential for early cancer diagnosis, particularly serving as a non-invasive biomarker in lung and Gastric cancers (GC). As a therapeutic target, restoring miR-17 expression via targeted interventions enhances. The efficacy of chemotherapy or targeted therapy thereby improves patient prognosis. Despite extensive research in this field, the precise mechanism of action for miR-17 remains incompletely understood. This review summarizes the current state of research concerning the relationship between miR-17 and its target genes in MT, as well as the underlying mechanisms involved.