miR-27a-3p overexpression

Finally, Sprouty2 (SPRY2) was verified to be the target gene of miR-27a-3p. In conclusion, activated HSC-derived sEVs with high levels of miR-27a-3p might induce M2 macrophage polarization and promote hepatoma progression, providing new insights into the mechanism of hepatoma progression.

Our study verified that LINC00891 attenuates the proliferation and metastasis of osteosarcoma cells via the miR-27a-3p/TET1 axis. This study clarifies a new mechanism and therapeutic target for the development of osteosarcoma.

Moreover, miR‑27a‑3p and TAB3 also activated the NF‑κB signaling pathway and formed a positive feedback regulatory loop composing of p65/miR‑27a‑3p/TAB3/NF‑κB. On the whole, the findings presented herein may provide novel insight into the underlying cervical tumorigenesis and novel biomarker identification for clinical applications.

miR-27a-3p is a major contributor to FTO downregulation in glioma under hypoxia. .

Above results suggest that the abnormally over-expressed miR-27a-3p in liver promotes the proliferation of cancer cells and accelerates the development of HCC by targeting inhibition the expression of USP46. Targeting miR-27a-3p may be an effective strategy for prevention and treatment of HCC.

Overexpressing miR-27a-3p led to SLC7A11 suppression via directly binding to its 3'-UTR, followed by the reduction of erastin-caused ferroptosis...Our literature collectively uncovered that miR-27a-3p modulated ferroptosis by targeting SLC7A11 in NSCLC cells, illustrating the important role of miRNA in ferroptosis. MiR-27a-3p modulates ferroptosis via targeting SLC7A11 in NSCLC cells, implying the significant role of miR-27a-3p/SLC7A11 in ferroptosis.

In summary, our findings report a new molecular mechanism for the miR-27a-3p-mediated Taxol resistance via targeting tumour suppressor, Fbxw7 in osteosarcoma. This study potentiates a miRNA-based therapeutic approach against Taxol resistant osteosarcoma.