MIR10A (MicroRNA 10a)

Its value also significantly correlated with the grade and stage of the tumor. Hence it can be concluded that urinary miRNA-10a is a potential candidate in the diagnosis and prognosis of UBC.

In vitro and in vivo experiments confirmed that miR-10a-5p-mediated downregulation of GATA6 suppressed Akt pathway activation. Overall, our findings suggest that miR-10a-5p could be a novel therapeutic target for ovarian cancer, and targeting the miR-10a-5p/GATA6/Akt axis could improve outcomes in this patient population.

Excitingly, the efficiency of α-d-Glu in promoting DC migration is not weaker than that of PGE2, which is the gold standard used to promote DC migration in clinical trials of DC vaccines. Thus, this study lays the foundation for further enhancing the objective clinical response rate of neoantigen vaccines and overcoming the limitation of an insufficient clinical response rate for neoantigen vaccines caused by low DC homing efficiency.

Moreover, LINRIS silencing inhibited cell proliferation, while miR-10a overexpression increased cell proliferation and inhibited the role of LINRIS silencing. Overall, LINRIS silencing may inhibit NSCLC cell proliferation by suppressing miR-10a maturation.Abbreviations: Non-small cell lung cancer (NSCLC); Reverse transcriptase-quantitative polymerase chain reaction (RT-qPCR); LncRNA long intergenic noncoding RNA for IGF2BP2 stability (LINRIS).

Furthermore, the transcriptional activity of FTO was inhibited by the transcription factor SPI1, which could be specifically disrupted by the SPI1 inhibitor DB2313. Treatment with this inhibitor restored endogenous FTO expression and decreased GBM tumor burden, suggesting that FTO may serve as a novel prognostic indicator and therapeutic molecular target of GBM.

Notably, miR-10a-5p mimic-modified HGC-27 exo enhanced the viability, migration and tube formation ability of HUVECs, but this effect was impaired after up-regulating ZMYND11. In summary, miR-10a-5p from GC cells-derived exo enhances viability and migration of HUVECs by suppressing ZMYND11.

 DEX can reduce postoperative OS and plasma miR-10a level in patients with lung cancer, and high expression of miR-10a predicts a high incidence of postoperative pulmonary complications.