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The present study aimed to explore the function of miR‑34b promoter methylation in cell proliferation in children's acute leukemia. Quantitative PCR and methylation‑specific PCR were performed to measure the levels of miR‑34b and its promoter methylation in normal cells, eight leukemia cell lines as well as primary leukemic cells isolated from patients newly diagnosed with acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML) and mixed lymphocytic lymphoma. miR‑34b levels in leukemia cell lines and primary leukemic cells were significantly lower than those in normal cells. The miR‑34b promoter was found to be methylated in all leukemia cell lines, 24 of 31 ALL patients and 8 of 19 AML patients, but not in the 23 normal controls. miR‑34b expression and methylation of its promoter were not associated with most clinical parameters assessed; however, miR‑34b levels in prednisone‑sensitive ALL were significantly different from those in insensitive ALL. A cell counting kit‑8 assay showed that transfection of miR‑34b mimics into K562 cells inhibited their proliferation. Furthermore, treatment with the demethylating agent 5‑aza‑2‑deoxycytidine significantly enhanced miR‑34b expression levels and decreased the methylation status of its promoter in HL‑60 and K562 cells. In conclusion, the results of the present study indicated that in pediatric leukemia cells and leukemia cell lines, the expression of miR‑34b is inhibited by methylation of its promoter, which impairs the restraining effects of miR‑34b on cell proliferation. It was also indicated that the expression of miR‑34b in ALL patients may affect their response to early treatments.

The aim of the present study was to investigate the effect of microRNA 146a (miR146a) on promoting the repair of corneal alkali burn with bone marrow mesenchymal stem cells (MSCs). A total of 24 Sprague‑Dawley female rats were divided into a normal group (Control), a normal MSC treatment group (Normal MSCs), an miR146a knockout MSC treatment group (miR146a‑low MSCs) and an miR146a high‑expression MSC treatment group (miR146a‑high MSCs) according to the random number table. Quantitative polymerase chain reaction was used to evaluate the expression levels of miR146a. MTT assay was performed to measure the cell viability of mesenchymal stem cells (MSCs) and apoptosis was measured by flow cytometry. The expression levels of p65 nuclear factor (NF)‑κB, proliferating cell nuclear antigen (PCNA) and Fas proteins were analyzed by western blotting. MSCs were tested for the secretion levels of vascular endothelial growth factor (VEGF), CD45, interferon (IFN)‑γ and interleukin (IL)‑10 by ELISA. The miR146a‑high MSCs improved cell viability of MSCs and inhibited apoptosis of MSCs following alkali burn. miR146a‑high MSCs decreased the expression levels of p65NF‑κB and PCNA, and enhanced the expression level of Fas. Furthermore, miR146a‑high MSCs improved the cornea opacity and enhanced the inhibition of neovascularization in the rats following alkali burn. miR146a‑high MSCs inhibit the expression of VEGF, CD45, IFN‑γ, while enhanced the expression of IL‑10. Therefore, miR146a promotes the repair of corneal alkali burn in rats treated with MSCs.

Trichohepatoenteric syndrome (THES) is a rare autosomal, recessively inherited disorder. Mutations in the tetratricopeptide repeat domain 37 (TTC37) gene and the superkiller viralicidic activity 2‑like (SKIV2L) gene have been identified to cause THES. The present study reported a case of a Chinese boy, who presented clinically with intrauterine growth retardation, intractable diarrhea, facial dysmorphism, abnormal scalp hair shafts, immune disorders and liver involvement. Targeted next‑generation sequencing and Sanger DNA sequencing showed compound heterozygous mutations of the SKIV2L gene. The present study was the first, to the best of our knowledge, to report a case of a boy with THES resulting from compound heterozygous mutations of the SKIV2L gene in China. Target sequence capture combined with high‑throughput next‑generation sequencing technologies have shown to be effective methods for the molecular genetic assessment of rare inherited disorders.

The histone deacetylase (HDAC) family is comprised of enzymes, which are involved in modulating the majority of critical cellular processes, including transcriptional regulation, apoptosis, proliferation and cell cycle progression. However, the biological function of HDAC5 in Wilms' tumor remains to be fully elucidated. The present study aimed to investigate the expression and function of HDAC5 in Wilm's tumor. It was demonstrated that the mRNA and protein levels of HDAC5 were upregulated in human Wilms' tumor tissues. Overexpression of HDAC5 in G401 cells was observed to significantly promote cellular proliferation, as demonstrated by the results of an MTT assay and bromodeoxyuridine incorporation assay. By contrast, HDAC5 knockdown using small interfering RNA suppressed the proliferation of the G401 cells. At the molecular level, the present study demonstrated that HDAC5 promoted the expression of c‑Met, which has been previously identified as an oncogene. In addition, downregulation of c‑Met inhibited the proliferative effects of HDAC5 in human Wilms' tumor cells. Taken together, these results suggested that HDAC5 promotes cellular proliferation through the upregulation of c‑Met, and may provide a novel therapeutic target for the treatment of patients with Wilms' tumor.