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SFRP2 was over-represented in a subset of multipotent BMSCs, which recreated a bone/marrow organ in an in vitro ectopic bone formation assay in a previous transcriptomic study. In models of skeletal organogenesis and regeneration, we investigated Sfrp2 deficiency on BMSC/SSC function. According to Sfrp2 KO Sfrp2 KO BMSCs/SSCs, there were less trabecular bone from WT littermates in the ectopic bone formation assay. Sfrp2 has revived the bulk of these operations, implying that Sfrp2 is a Wnt agonist. We show that Sfrp2 is involved in the self-renewal of SSCs and the selection and differentiation of adult SSCs during bone healing. SFRP2 is also a useful indicator of BMSC/SSC multipotency and a measure of potential improvement of ex vivo expanded BMSC/SSC products.
Source link: https://doi.org/10.1038/s41413-021-00169-7
Introduction Breast cancer is one of the most common female cancers globally, in which cancer stem cells play essential roles. Circular RNAs have received a lot of attention in the cancer research field, and propofol, a commonly used intravenous anesthetic agent, is widely used. Methods: We reviewed the role of circular RNA nucleolar and coiled-body phosphoprotein 1 in breast cancer CSCs, as well as the inhibitory effects of propofol on circNOLC1. Conclusions Compared to the non-tumor tissues, circNOLC1 was activated in breast cancer tissues. The silencing of circNOLC1 was able to reduce the viability of breast cancer cells. Breast cancer cells' invasion and migration capability was reduced by the inhibition of circNOLC1. The repression of circNOLC1 decreased the breast cancer cell population ratio. Meanwhile, the silencing of circNOLC1 has reduced breast cancer cells' ability. CirNOLC1 served as a competing endogenous RNAs for microRNA-365a-3p and miR-365a-3p inhibition enabled circNOLC1 depletion-repressed proliferation and breast cancer stem cell expression, according to the mechanism. By sponging MiR-365a-3p, a targeted signal transducer and transcription 3 inducer in breast cancer cells and circNOLC1 increased STAT3 expression in breast cancer cells and circNOLC1. STAT3's overexpression could cause miR-365a-3p or circNOLC1 depletion-inhibited proliferation and breast cancer stem cell properties. Conclusions By repressing STAT3 in a feedback system, we discovered that circNOLC1 contributes to CSCs properties and breast cancer progression, as well as breast cancer progression.
Source link: https://doi.org/10.1186/s12967-021-03133-5
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