miR‑106-a expression

Finally, restoration of miR-106a-5p in NORAD-overexpressing CRC cells re-sensitized cisplatin resistance by targeting CCND1. Summarily, this study uncovered a NORAD-promoted cisplatin resistance through modulating the miR-106a-5p-CCND1 axis, contributing to developing novel therapy for treating chemoresistant CRC.

Luteolin treatment led to a reduction in A549 cell migration, and this reduction was further amplified by the overexpression of miR-106a-5p. Luteolin inhibits A549 cell migration by modulating the miRNA landscape, shedding light on its mechanisms and laying the foundation for miRNA-based therapeutic approaches for NSCLC.

Furthermore, miR-106a overexpression suppressed RB cell angiogenesis by downregulating HIF-1α expression level. NEAT1 promoted proliferation, invasion, and angiogenesis of RB cells through upregulation of HIF-1α expression level by sponging miR-106a, demonstrating that NEAT1 may be a novel target for RB treatment.

PWAR6 restrained cell growth, migration and invasion of glioma, which was alleviated by the overexpression of microRNA-106a-5p (miR-106a-5p). PWAR6 functioned as a prognostic biomarker and tumor suppressor of glioma through regulating miR-106a-5p.

miR-106a-5p is a tumor suppressor that negatively regulates GPR133. The miR-106a-5p/GPR133 axis could potentially serve as a therapeutic target for glioma.

Further, we found that miR-106-5a is bound with 3'-UTR of AKT interacting protein (AKTIP) mRNA specifically, and then activate PI3K/AKT/m-TOR pathway in LC cells. A new mechanism was uncovered that miR-106a-5p promotes LC development via AKTIP/PI3K/AKT/m-TOR axis, which guides clinical management and drug discovery.

High expression of miR-106a assists the diagnosis of HPV-positive CC and predicts poor prognosis.

This study provides a framework of co-expression gene modules and miRNAs of CRC, which identifies some important biomarkers for CRC pathogenicity and diagnosis. Further experimental evidence will be required to support this study and validate the precise molecular pathways.

Importantly, apelin blockade inhibits prostate cancer metastasis in the orthotopic mouse model. Thus, apelin is a promising therapeutic target for curing metastatic prostate cancer.

Exosomal miR-106a-5p accelerated the progression of NPC through the FBXW7-TRIM24-SRGN axis. Our study elucidates novel regulatory mechanisms of NPC progression and provides potential exosome-based therapeutic strategies for NPC.

Raji-Evs-carried miR-106a inhibited Beclin1-dependent autophagy and apoptosis in lymphoma cells, which were further verified in vivo, together with promoted tumor growth. We proved that Raji-Evs inhibited lymphoma cell autophagy and apoptosis and promoted cell growth via the miR-106a/Beclin1 axis.

EVs-miR-106a-5p facilitated OC metastasis via the KLF6/PTTG1 axis. To conclude, OC cell-derived EVs facilitated the progression and metastasis of OC via the miR-106a-5p/KLF6/PTTG1 axis.