miR-10b overexpression

RMST silencing could attenuate inflammatory response and cardiomyocyte apoptosis and upregulate cardiac function in mice with doxorubicin-induced HF by modulating the miR-10b-5p/TRAF6 axis. The study provides novel therapeutic targets for HF treatment.

miR-10b-5p facilitates the metabolic reprogramming of PLC by targeting SLC38A2, which ultimately boosts the proliferation, migration, and invasion of PLC cells. Therefore, miR-10b-5p and SLC38A2 are potential targets for PLC diagnosis and treatment.

Moreover, miR‑10b‑5p increased the number of cells in the G phase. In conclusion, tumor‑suppressive miR‑10b‑5p was significantly downregulated in ULMS compared with in myoma; thus, miR‑10b‑5p may serve a specific role in sarcoma progression.

Although more clinical validations are needed for the diagnosis of HCC, our current results indicate that the coexistence of high expression of miR-10b and miR-24 may help clinicians adjust in the diagnosis of HCC in patients who are on the liver transplant list but awaiting biopsy for the diagnosis of HCC.

In summary, miR-10b-5p delivered by hypoxic glioma-derived EVs accelerated macrophages M2 polarization to promote the progression of glioma via NEDD4L/PIK3CA/PI3K/AKT axis.

DEX pretreatment elevated BDNF expression by reducing miR-10b-5p expression, thereby alleviating ropivacaine-induced neurotoxicity.

Notably, animal experiments confirmed that miR-10b-Bim promoted proliferation and autophagy in OSCC. In addition, this study provides a theoretical support for regulating the mechanism of OSCC by inducing autophagy with miR-10b-Bim as a target.

This study not only identified the molecular target for miR-10b-3p, but also provided evidence that circulating miR-10b-3p may be used as a biomarker for predicting sorafenib sensitivity in patients with HCC.

LncRNA GAS5 interacts with miR-10b to inhibit cell proliferation and migration and induces apoptosis in colorectal cancer. GAS5 and miR-10b could become potential therapeutic targets for CRC.

Furthermore, dual luciferase reporter assay verified that miR-10b-5p was a target of EphA2, and the rescue experiment implied that transfection of pCMV-EphA2 or Si-EphA2 could reverse EphA2 expression and cell biological functions caused by miR-10b-5p overexpression or knockdown. miR-10b-5p reduced HCC cell proliferation but accelerate apoptosis by regulating EphA2, suggesting it has the potential to be a clinical target for HCC.

Besides, KLF5 was identified as a target of miR-10b-3p, and rescue experiments revealed that KLF5 was involved in the regulation of miR-10b-3p in ischemic injury. Our results demonstrated that miR-10b-3p had the neuroprotective effects against ischemia injury by targeting KLF5 and provided a potential underlying target for ischemic stroke treatment.

Our results indicated that miR-10b could act as a significant biomarker in the prognosis DSCs. However, more research should be performed to test these findings.