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Protective role of lncRNA HOXB-AS3 in doxorubicin (DOX)-induced cardiotoxicity and its mechanism were studied. Viability of PC and H9c2 cells treated with different doses of DOX was determined through CCK-8 assay. Relative level of HOXB-AS3 in DOX-treated cardiomyocytes was detected. Regulatory effect of HOXB-AS3 on the proliferative ability of DOX-treated cardiomyocytes was assessed. Through dual-luciferase reporter gene assay, the binding relationship between HOXB-AS3 and miRNA-875-3p was verified. Rescue experiments were conducted to explore the role of HOXB-AS3/miRNA-875-3p in influencing the proliferation of DOX-treated cardiomyocytes. The proliferative ability of cardiomyocytes was dose-dependently downregulated after DOX treatment. Relative level of HOXB-AS3 was upregulated in DOX-treated cardiomyocytes. Silence of HOXB-AS3 in cardiomyocytes undergoing DOX treatment markedly elevated their proliferative ability. miRNA-875-3p was the direct target of HOXB-AS3. Knockdown of miRNA-875-3p reversed the role of HOXB-AS3 in regulating the proliferative ability of cardiomyocytes. HOXB-AS3 protects DOX-induced suppression in the proliferation of cardiomyocytes through targeting and downregulating miRNA-875-3p.

lncRNA HOXB‑AS3 protects doxorubicin‑induced cardiotoxicity by targeting miRNA‑875‑3p