Apigenin, a naturally occurring flavonoid, is known to exhibit antitumor activity in many cancers. However, the regulatory mechanism of apigenin and the long noncoding RNAs (lncRNAs) altered upon apigenin treatment in oral squamous cell carcinoma (OSCC) remain unclear. In this study, we found that LINC00629 was significantly upregulated in response to apigenin treatment. Upregulated LINC00629 enhanced the growth-suppressive and proapoptotic effects of apigenin on OSCC cells by interacting with Mcl1 and facilitating its degradation. Subsequently, our data indicated that KLF10, an important transcription factor, directly bound to the promoter of LINC00629, facilitating its transcription and contributing to apigenin-induced LINC00629 expression. Collectively, these results suggest that the KLF10-LINC00629-Mcl1 axis plays an important role in the anticancer effects of apigenin.
BackgroundSmall extracellular vesicles (sEVs) are an important component in the paracrine pathway. They can be used as a substitute for seed cells and have shown good application prospects in promoting bone regeneration. Cow’s milk could be used as a source of sEVs with good biocompatibility and cost-effectiveness, with easy availability, low cost and low toxicity. This study focused on the role and mechanism of small extracellular vesicles derived from milk in bone repair.MethodssEVs were isolated from fresh milk by ultracentrifugation, and the extraction of Milk-sEVs was identified by TEM, NTA, and Western blotting. The effects of Milk-sEVs on the proliferation and differentiation of osteoblasts were studied by CCK-8 assay, ALP, Western blotting and Real-time PCR. A mice skull defect model was constructed, and the bone formation at the defect site was observed by HE staining, Masson staining and IHC. The differential gene GJA1 after Milk-sEVs acted on osteoblasts was screened by transcriptome chip, and the transcript AP3B1 of GJA1 was verified by CHIP.ResultsWe have proved by in vivo and in vitro experiments that milk-derived sEVs (Milk-sEVs) increase the repair ability of bone tissue, and promote expression of the osteogenic gene GJA1 through the transcript AP3B1.ConclusionMilk-sEVs can enhance the expression of the transcription factor AP3B1, AP3B1 can bind to the GJA1 promoter to enhance the expression of GJA1 and promote bone repair.
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