MIR188 (MicroRNA 188)

Clinical validation using TCGA data confirmed elevated RBP-J and miR-188-5p expression, alongside reduced TIMP2/3 levels, as prognostic biomarkers for poor CRC outcomes. These findings reveal a novel Notch-miR-188-5p-TIMP2/3 signaling cascade driving exosome-mediated PMN formation, offering insights into therapeutic strategies targeting the metastatic microenvironment.

See also the graphical abstract(Fig. 1).

Lower expression of exomiR-188-3p predicted a poor overall survival and progression-free survival in patients with OC. Decreased exomiR-188-3p could be a potential early diagnostic and prognostic biomarker for OC patients.

More innovatively, the potential of circTNPO3 as a novel diagnostic biomarker and therapeutic target for PC was primarily validated in present study. CircTNPO3 acted as an oncogenic and chemoresistant gene in PC, mechanically through targeting miR-188-5p and regulating CDCA3, TRAF2 and NF-κB signaling pathway.

In conclusion, α‑radiation induced distinct proteomic, lipidomic and miRNA changes in OBCs, potentially affecting BM radiosensitivity. These molecules may serve as candidate biomarkers for predicting individual susceptibility to α‑emitting radionuclide therapy.

Mast cell-derived exosomes, particularly those from activated cells (AE), exacerbated ECM neuronal injury through partial activation of ER stress pathways.

circQKI drives DTX resistance via the miR-188-3p/Beclin-1 axis and autophagy activation, with its expression regulated by METTL3-dependent m6A modification and IGF2BP2. Targeting circQKI or autophagy pathways may offer novel therapeutic strategies to overcome DTX resistance in prostate cancer.

Exosomal miR-188-3p derived from CRC cells can promote liver metastasis by activating HSCs to form a PMN through targeting PHLPP2 to activate the AKT/mTOR pathway. These results offer a new perspective on the mechanisms driving CRLM.

Our results suggest that miR-188-5p acts as an oncomiRNA in CML pathogenesis and may be a promising therapeutic target for CML.

Sodium cromoglycate (SCG) is a membrane stabilizer for MCs and confirmed as an effective and widely used agent to block TAMCs-derived CXCL10 and further sensitize the therapeutic efficacy of anti-PD-1 antibody plus gemcitabine for PDAC. These findings illuminate a critical and innovative crosstalk between TAMCs and PDAC cells that promote PDAC progression, and SCG sensitizes PDAC to the current immuno-chemotherapy, which reveals its potential to be a valuable adjuvant for PDAC patients.

These findings both reinforce our current understanding of prostate cancer's molecular landscape and point to unexplored pathways that could lead to novel therapeutic strategies. By mapping these regulatory relationships, our work contributes to the growing knowledge base needed for developing more targeted and effective treatments.