MicroRNAs (miRs) exhibit oncogenic or tumor suppressive functions that contribute to the initiation and development of various types of human cancer. miR‑149‑3p has been reported to serve multiple roles in the regulation of proliferation, apoptosis and metastasis. However, the effects and detailed mechanism of miR‑149‑3p in oral squamous cell carcinoma (OSCC) remain unclear. In the present study, miR‑149‑3p mimic, mimic control, miR‑149‑3p inhibitor and inhibitor control were transiently transfected into Cal27 and SCC‑9 cells. The viability, proliferation and apoptosis of OSCC cells were determined using Cell Counting Kit‑8, colony formation and Annexin V assays, respectively. The mRNA expression levels of miR‑149‑3p and AKT2 were determined by reverse transcription‑quantitative PCR. The protein expression levels of AKT2, cleaved caspase‑3 and cleaved PARP were examined by western blot analysis. The binding of miR‑149‑3p to the AKT2 3'‑untranslated region was evaluated by a dual luciferase reporter assay. In .Subsequently to the publication of this paper, an interested reader drew to the authors' attention that, in Fig. 1A on p. 524, the images selected to represent the Control experiments for the SU‑DHL‑8 and OCI‑Ly01 cell lines bore some striking similarities. After having examined their original data, the authors realized that they uploaded the wrong images during the process of compiling this figure. The corrected version of Fig. 1, showing the correct data for Fig. 1A, is shown on the next page. Note that the replacement of the erroneous data does not affect either the results or the conclusions reported in this paper, and all the authors agree to this Corrigendum. The authors are grateful to the Editor of Molecular Medicine Reports for granting them this opportunity to publish a Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Molecular Medicine Reports 17 522‑530, 2018; DOI 10.3892/mmr.2017.7892].Radiation therapy, one of the major treatment options for cancer, can cause delayed heart damage. The circular RNA (circRNA) circFOXO3 (hsa_circ_0006404) is associated with cancer progression. However, the functions of circFOXO3 in radiation‑induced cardiotoxicity remains unknown. The present study aimed to identify the functions of cirFOXO3 in radiation‑induced cardiotoxicity. The present study established circFOXO3‑knockdown (KD) or ‑overexpressing (OE) cardiomyocytes. Functional assay results showed that KD of circFOXO3 in cardiomyocytes significantly increased DNA damage and apoptosis after radiation. By contrast, OE of circFOXO3 reduced DNA damage and apoptosis rates in response to radiation. Mechanistically, KD of circFOXO3 elevated the levels of Bax, caspase 3 and caspase 7, and decreased Bcl‑2 expression, whereas OE of circFOXO3 decreased Bax, caspase 3 and caspase 7 expression, and increased Bcl‑2 expression. Thus, the present study indicated that circFOXO3 protected cardiomyocytes from radiation‑induced cardiotoxicity by reducing DNA damage and apoptosis. circFOXO3 may be a potential therapeutic target against radiation‑induced cardiotoxicity.Endotoxin lipopolysaccharide (LPS) is one of the primary causes of myocardial injury. Propofol confers protective effects against LPS‑induced myocardial damage; however, the biological functions and mechanisms underlying propofol are not completely understood. The present study aimed to investigate the effects of propofol on LPS‑induced myocardial injury. Primary neonatal rat cardiomyocytes were treated with LPS to establish a myocardial injury model. LDH release in the culture media was measured using a LDH assay kit. The interactions between NLR family pyrin domain containing 3 (NLRP3), apoptosis‑associated speck‑like protein containing A CARD (ASC) and pro‑caspase‑1 were determined using a co‑immunoprecipitation assay. Cell viability was measured using an MTT assay, and the levels of cell apoptosis were determined using flow cytometry, JC‑1 staining (mitochondrial membrane potential) and caspase‑3 activity assays. The mRNA expression levels of TNF‑α, IL‑6, IL‑1β and IL‑18, and the protein expression levels a potential therapeutic agent for septic myocardial damage.Myocardial ischemia/reperfusion (MIR) injury, which occurs following acute myocardial infarction, can cause secondary damage to the heart. https://www.selleckchem.com/products/mk-8353-sch900353.html Tripartite interaction motif (TRIM) proteins, a class of E3 ubiquitin ligases, have been recognized as critical regulators in MIR injury. Zenglv Fumai Granule (ZFG) is a clinical prescription for the treatment of sick sinus syndrome, a disease that is associated with MIR injury. The present study aimed to investigate the effect of ZFG on MIR injury and to determine whether ZFG exerts its effects via regulation of TRIM proteins. In order to establish an in vitro MIR model, human cardiomyocyte cell line AC16 was cultured under hypoxia for 5 h and then under normal conditions for 1 h. Following hypoxia/reoxygenation (H/R) treatment, these cells were cultured with different ZFG concentrations. ZFG notably inhibited H/R-induced cardiomyocyte apoptosis. The expression levels of four TRIM proteins, TRIM7, TRIM14, TRIM22 and TRIM28, were also detected. These four proteins were significantly upregulated in H/R-injured cardiomyocytes, whereas their expression was inhibited following ZFG treatment. Moreover, TRIM28 knockdown inhibited H/R-induced cardiomyocyte apoptosis, whereas TRIM28 overexpression promoted apoptosis and generation of reactive oxygen species (ROS) in cardiomyocytes. However, the effects of TRIM28 overexpression were limited by the action of ROS inhibitor N-acetyl-L-cysteine. In addition, the mRNA and protein levels of antioxidant enzyme glutathione peroxidase (GPX)1 were significantly downregulated in H/R-injured cardiomyocytes. TRIM28 knockdown restored GPX1 protein levels but had no effect on mRNA expression levels. Co-immunoprecipitation and ubiquitination assays demonstrated that TRIM28 negatively regulated GPX1 via ubiquitination. In sum, the present study revealed that ZFG attenuated H/R-induced cardiomyocyte apoptosis by regulating the TRIM28/GPX1/ROS pathway. ZFG and TRIM28 offer potential therapeutic options for the treatment of MIR injury.