2023
DOI: 10.1016/j.mcp.2023.101937
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Long noncoding RNA RMRP ameliorates doxorubicin-induced apoptosis by interacting with PFN1 in a P53-Dependent manner

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Cited by 4 publications
(2 citation statements)
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“…In conclusion, morphological and functional defects of the heart in doxorubicin-induced cardiotoxicity are similar to those of DCM [19,20]. Meanwhile, according to the previous study [21], the HL-1 and AC16 cells were respectively administrated with Dox (0.5µmol/L) for 24 h. As shown in Fig. 2F-2H, we found that doxorubicin administration promoted the enlargement of cardiac cells and enhanced the mRNA levels of cardiac hypertrophic genes.…”
Section: Doxorubicin-induced Cardiotoxicity In Vitro and In Vivo Modelsupporting
confidence: 68%
“…In conclusion, morphological and functional defects of the heart in doxorubicin-induced cardiotoxicity are similar to those of DCM [19,20]. Meanwhile, according to the previous study [21], the HL-1 and AC16 cells were respectively administrated with Dox (0.5µmol/L) for 24 h. As shown in Fig. 2F-2H, we found that doxorubicin administration promoted the enlargement of cardiac cells and enhanced the mRNA levels of cardiac hypertrophic genes.…”
Section: Doxorubicin-induced Cardiotoxicity In Vitro and In Vivo Modelsupporting
confidence: 68%
“…Wang et al observed that knockdown of SOX2-OT downregulated DP5 via sponging miR-942-5p and inhibiting DOX-induced apoptosis in primary cardiomyocytes [ 83 ]. Gong et al showed that overexpression of lncRNA RMRP could inhibit the expression of p53 and its phosphorylation level by suppressing profilin 1 (PFN1) to exert cardioprotective effects, holding great promise for serving as a therapeutic target and potential biomarker of DIC [ 86 ]. In the DIC in vitro model, DOX treatment resulted in the upregulation of methyltransferase-like 14 (METTL14), which catalyzed the m6A modification of lncRNA KCNQ1OT1, a miR-7-5p sponge [ 79 ].…”
Section: Non-coding Rnas Involved In the Dicmentioning
confidence: 99%