[γδ1 T cells derived from breast cancer tissue induce immunosenescence of naive CD4 T cells by producing IL-17D].

Objective To investigate the mechanism underlying the immunosuppressive effect and its reverse of γδ1 T cells derived from breast cancer tissues by inducing immunosenescence. Methods After γδ1 T cells isolated from breast cancer tissues were co-cultured with peripheral blood-derived naive CD4 T cells, the proliferation of treated CD4 T cells was detected by CCK-8 assay, and the activity of senescence-associated β-galactosidase (SA-β-Gal) in treated CD4 T cells was detected by SA-β-Gal staining. After the induced senescent CD4 T cells were co-cultured with the naive CD4 T cells, the proliferation, apoptosis, activity of the treated CD4 T cells were examined by CCK-8 assay, flow cytometry and SA-β-Gal staining, respectively; the expression of cell cycle-associated proteins P53, P21 and P16 in the treated CD4 T cells was detected by Western blot analysis in order to verify the immunosuppressive effect of the senescent CD4 T cells.

miR-873 suppresses H9C2 cardiomyocyte proliferation by targeting GLI1.

MicroRNAs (miRNAs) are a class of endogenous, non-coding small RNAs that regulate the expression of target genes. Previous studies have suggested that miRNAs are key regulators in cardiovascular systems. This study investigated the role of miR-873 in H9C2 cardiomyocytes by targeting glioma-associated oncogene 1 (GLI1).