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Conversely, overexpression of FOXD2-AS1 promoted tumor growth in vitro. Mechanistically, FOXD2-AS1 inversely regulated miR-324-3p abundance in hemangioma cells. We also found FOXD2-AS1 acted as a competing endogenous RNA (ceRNA) by directly sponging miR-324-3p to regulate PDRG1 expression. In addition, the knockdown of PDRG1 reversed the stimulation effects of FOXD2-AS1 overexpression on HA cells. Conclusion To conclude, our study sheds novel light on the biological roles of FOXD2-AS1 in hemangioma, which may help the development of targ
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