MIR33 (MicroRNA 33)

This study bridged miRNomic and lipidomic data in relevant mouse models, allowing to highlight novel miRNAs potentially playing a role in the modulation of lipid levels.

This is the first study to provide insights into the FGT miRNA profiles following Nb and HSV-2 single and co-infection, as well as the predicted genes and pathways they regulate, which may influence host immunity and pathology. This study highlights the role of miRNAs in regulating FGT immunity and pathology in the context of STH/HSV-2 co-infection.

Moreover, miRNA-based therapeutic strategies, including antagomirs and miRNA mimics, hold promise for targeted intervention in both diseases, which could reduce ASCVD risk in cancer patients and improve long-term outcomes. Understanding the intricate interactions between miRNAs, lipid metabolism and disease progression provides new insights into the overlapping molecular mechanisms of cancer and ASCVD and opens new therapeutic opportunities in the field of cardio-oncology.

Our findings suggest that c-Myc and LncRNAs (TCF7L2, PVT1, and CCAT2) are upregulated and miR-33 is downregulated in OSCC compared to OLP samples. These genes may serve as potential genetic biomarkers for diagnosis and prediction of clinicopathological features of OSCC.

HDAC1/FOXK1 upregulation and miR-33a silencing are new mechanisms of EGFR-TKI resistance in NSCLC.

The reduction in lipid accumulation and liver injury resulted in decreased YAP/TAZ pathway activation, which may be involved in the reduced HCC progression in HKO livers. Together, these results suggest suppressing hepatic miR-33 may be an effective therapeutic approach to temper the development of NAFLD, NASH, and HCC in obesity.

We propose several potential mRNA targets and hypothetical mechanisms by which each microRNA exerts its effect. We hereby open new perspectives in the research on OPC differentiation and the pathophysiology of demyelination/remyelination, and possibly even in the search for new remyelinating therapeutic strategies in the scope of MS.

In our CG4 transfection model, MS-related microRNAs can reduce OPC differentiation. We are currently investigating their messenger RNA targets to unravel the underlying signalling pathways involved. These results are encouraging to understand remyelination defects in MS.

In conclusion, this study showed that miR-33-3p regulated Slc29a1, which in turn controlled the proliferation and differentiation of PC12 cells. Thus, we hypothesize that the miR-33-3p/Slc29a1 axis could be a promising therapeutic target for recovering neurons and the cholinergic nervous system.

SelT overexpression could ameliorate the increase in apoptosis induced by hsa-miR-33-5p mimics. Our findings revealed that hsa-miR-33-5p, as a potential therapeutic target, could accelerate breast cancer cell apoptosis.

So, our data suggests that exosomes can be used as an efficient nanocarrier for miR-33 delivery into macrophages. Also, miR-33 is capable of inducing M1 polarization in macrophages, which is essential for suppressing tumor growth and metastasis.