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The expression of miR‑142‑3p was significantly increased while AC9 and cAMP expression significantly decreased in CCI rats. However, AC9 overexpression significantly increased the levels of cAMP protein. HC-258 solubility dmso Luciferase reporter assay also proved that AC9 is the target gene of miR‑142‑3p. Moreover, miR‑142‑3p silencing was found to reduce neuropathic pain in CCI rats by upregulating the expression of AC9. It was also found that cAMP activation can relieve neuropathic pain and promote the expression of AMPK‑related proteins in CCI rats. Silencing miR‑142‑3p can target AC9 to reduce the expression of inflammatory factors and neuropathic pain in CCI rats by increasing the expression of cAMP/AMPK pathway‑related proteins.Bone marrow mesenchymal stem cells (BMSCs) are accepted as a form of cellular therapy to improve cardiac function following acute myocardial infarction (AMI). The present study was performed to investigate the synergistic effect of ultrasound‑targeted microbubble destruction (UTMD)‑mediated Galectin‑7‑small interfering (si)RNA with the homing of BMSCs for AMI. The rat model of AMI was established, followed by identification of BMSCs. Rats with AMI received BMSC transplantation, BMSC transplantation + UTMD + siRNA negative control, or BMSC transplantation + UTMD + Galectin‑7‑siRNA. The cardiac function, hemodynamics indexes, degree of myocardial fiber injury and expression of apoptosis‑related proteins in myocardial tissues of rats were detected. The homing of BMSCs was observed, and the indexes of myocardial microenvironment and the TGF‑β/Smads pathway‑related proteins in myocardial tissues were determined. AMI rats treated with UTMD‑mediated Galectin‑7‑siRNA exhibited improved cardiac function and hemodynamics‑related indices, decreased myocardial fiber injury and apoptotic cells, as well as enhanced homing ability of BMSCs, improved myocardial microenvironment, and suppressed TGF‑β1/Smads pathway activation. In conclusion, the present study demonstrated that UTMD‑mediated Galectin‑7‑siRNA treatment could enhance the homing ability of BMSCs, thus alleviating AMI in rats.TP53 is the most common gene mutated in human cancers, including in cholangiocarcinoma (CCA). The gain‑of‑function properties of p53 variants are often involved in cancer progression. The present study demonstrated that a truncated del p53 variant, del p53M213, exhibited gain‑of‑function properties and was highly expressed in the invasive liver fluke Opisthorchis viverrini‑associated CCA cell line, KKU‑M213. The del p53M213 variant lacked exons 7‑9 and contained a V31I substitution (p53‑p72‑Δ225‑331‑V31I). Stably transfected p53‑null human non‑small cell lung H1299 cells exhibited a del p53M213 localization in both the cell cytosol and nucleus. Del p53M213 lacked anti‑growth functions, and instead enhanced migration and invasiveness. In addition, this p53 variant downregulated claudin‑1 expression and promoted Cdc42 activation, consistent with the roles of claudin‑1 and Cdc42 in inhibiting cell‑cell dissociation and promoting cell migration, respectively. On the whole, although del p53M213 is an important driver of cancer cell migration and invasiveness, other properties related to its novel gain‑of‑function properties require further investigation in order to develop effective treatment strategies for cancers bearing this truncated TP53 allele.Breast cancer is the most frequently diagnosed malignancy and leading cause of cancer-related deaths among women worldwide. Tumor recurrence, or metastasis, is caused by cancer stem cells and has a dismal prognosis for breast cancer patients. Thus, targeting breast cancer stem cells (BCSCs) for eradication is a potential method to improve clinical outcomes. Phenethyl isothiocyanate (PEITC) is a novel epigenetic regulator derived from cruciferous vegetables that has marked antitumor effects. However, the exact mechanism of these antitumor effects by PEITC is unknown. As breast cancer progresses, a tumor suppressor in the breast, cadherin 1 (CDH1), is silenced by hypermethylation of the promoter region, further promoting the stem cell-like properties of cancer. Herein, the ability of PEITC to reduce BCSC-like properties by epigenetic reactivation of CDH1 was investigated by multiple analyses such as MTT, colony formation and sphere formation assays, methylation-specific PCR, western blot analysis, Co-IP and qPCR. It was revealed that PEITC inhibited colony and mammosphere formation and decreased the expression of protein markers associated with BCSC-like properties via epigenetic reactivation of CDH1. Further exploration of this mechanism revealed inhibitory effects of PEITC on DNMTs and HDACs, which play a pivotal role in demethylating the hypermethylated CDH1 promoter region. Reactivated CDH1 suppressed the Wnt/β-catenin pathway which confers BCSC-properties in breast cancer cells. These findings suggest a novel method to eradicate BCSCs from breast cancer patients.Following the publication of the above article, the authors noticed that data shown in certain of the panels in Figs. 4 and 5 were selected incorrectly and presented wrongly in these figures. Essentially, in Fig. 4, the data shown for the Tunel, anti‑EGFR‑iRGD and Tunel, anti‑EGFR‑iGRD+IR data panels (i.e., the panels in the third row, columns 2 and 4), were chosen incorrectly, and in Fig. 5, the data panel for the Lung, IR experiment (fourth row, third column) was selected incorrectly. The revised versions of Figs. 4 and 5, featuring all the correct data panels, are shown on the next page. Furthermore, the results were re‑analyzed based on the correct data. The errors made in the compilation of these Figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of Oncology Reports for allowing them the opportunity to publish this Corrigendum, and apologize to the readership for any inconvenience caused. [the original article was published in Oncology Reports 40 1583-1591, 2018; DOI 10.3892/or.2018.6532].