hsa-miR-let-7b-5p miREIA

Let-7b has been found to act as a tumor suppressor, in order to halt cell proliferation, adhesion, and invasion by targeting the genes of PKA1, DIAPH2, RDX, Ras, c-myc, and HMGA2 proteins. Let-7b expression is differently regulated in breast cancer and the data reveal its possible role in DNA repair capacity during breast carcinogenesis. Similarly, miR-let-7b was shown to be significantly downregulated in osteosarcoma tissues and cell lines and the functional studies revealed that the antitumor effect of miR-let-7b was probably due to targeting and suppressing IGF1R expression. Let-7b has differential expression patterns also in inflamed tissues compared with healthy controls. The data demonstrate that overexpression of miR-let-7b caused a marked decrease in the expression of the proinflammatory genes, whereas blocking of miR-let-7b caused a reciprocal increase in cytokine expression. Circulating miR-let-7b-5p together with miR-125b-5p function as regulators of the inflammatory response in endometriosis. It was published that up-regulation of miR-let-7b was characteristic of prostatic tumor-associated macrophages and might play a vital role in regulating macrophage polarization, thus modulating the prognosis of prostate cancer. Furthermore, results suggest that miR-let-7b contributes to the epithelial immune responses against H. pylori infection. It has also been shown that miR-let-7b may protect human mesenchymal stem cells implanted into infarcted myocardium from apoptosis and autophagy. Moreover, miR-let-7b has been linked to neurodegeneration; elevated amounts of miR-let-7b were found in the cerebrospinal fluid of patients with Alzheimer s disease. In addition, miR-let-7b might be a promising blood-derived miRNA biomarker in multiple sclerosis.