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This research was designed to investigate the role of MSC-derived exosomes in the stemness of hepatocellular carcinoma stem cells and the molecular mechanism. After Exo treatment, C5orf66-AS1 was discovered as the most upregulated long noncoding RNAs in CSCs. The restriction of Exo's control functions in the CSCs could not be prevented by either mechanical overexpression of miR-127-3p or silencing DUSP1. Exo reduced the growth of xenograft in nude mice by CSCs in nude mice, and this reduction was blocked until miR-127-3p overexpression or DUSP1 silencing.
Source link: https://doi.org/10.1007/s13577-021-00599-9
Oral tongue squamous cell carcinoma is a common form of oral carcinoma. In vitro, this study was designed to determine and compare the anticancer activity of three distinct magnetic selenium nanocomposites against tongue carcinoma stem cells. Cultured tongue carcinoma stem cells were divided into four groups by four groups. Cell proliferation in cell proliferation decreased at 24 h in groups I, III, and IV, according to MTT's analysis, only group II showed significant decline in cell proliferation at 24 h relative to groups I, III, and IV. However, cell proliferation in cell proliferation in the 48 hours, did decrease dramatically during 48 hours compared to the untreated group. In group II followed by group III at 48 h, the most apparent ultrastructural changes were apparent, with a cancer effect on tongue carcinoma stem cells in vitro.
Source link: https://doi.org/10.1007/s12668-021-00913-7
Co-IP, ubiquitination-IP, and ChIP assays tested CDK11B, SPDEF, miR-448, and DOT1L, respectively, while ChIP, ubiquitination-IP, and ChIP assays determined the correlation between CDK11B, SPDEF, miR-448, and DOT1L, whereas ChIP's effects on the biological characteristics of HCC stem cells were determined by sphere formation and colony formation and colony a An in vitro xenograft tumor model was developed to demonstrate that CDK11B is capable of regulating HCC stem cells' oncogenicity. SPDEF was degraded by theubiquitin-proteasome pathway, while SPDEF might attach to the miR-448 promoter and stop the production of DOT1L by activating miR-448, which also promotes self-renewal of HCC stem cells by encouraging self-renewal of HCC stem cells by increasing self-renewal of HCC stem cells. In vivo, Knockdown of CDK11B attenuated the self-renewal capability of HCC stem cells and their oncogenicity. These results showed that blocking the CDK11B-induced degradation of SPDEF and improving miR-448-dependent inhibition of DOT1L can slow HCC progression by hindering the development of HCC by decreasing self-renewal capability of HCC stem cells, which are new targets for HCC control.
Source link: https://doi.org/10.1038/s41417-020-00261-w
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