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In addition, following treatment with curcumin for 48 h, H19 expression was decreased in a dose‑dependent manner. Moreover, curcumin treatment for 48 h significantly attenuated H19‑induced alterations in N‑cadherin and E‑cadherin expression levels. Curcumin also prevented H19‑induced invasion and migration. The present study indicated that H19 may serve as a promoting factor of EMT, invasion and migration in MCF‑7/TAMR cells, suggesting that curcumin may prevent H19‑associated metastasis. Therefore, curcumin may serve as a promising therapeutic drug for patients with TAMR breast cancer.While radiation nephropathy is a major problem associated with radiotherapy, the exact mechanisms underlying its pathogenesis and the mediators involved in kidney deterioration remain to be elucidated. In view of the finding that senescence is typically increased post‑irradiation, the present study examined whether ionizing radiation may cause kidney injury by enhancing premature senescence. The present study explored the relevance of the aging suppressor, Klotho, which has anti‑aging activity and is highly expressed in murine renal cells/kidney tissues, under irradiation conditions. Firstly, the effects of radiation on mouse inner medullary collecting duct‑3 (mIMCD‑3) cells and kidney tissues of mice were assessed. Subsequently, the mRNA expression levels of Klotho, TNF‑α and ADAM metallopeptidase domain (ADAM)9/10/17 were analyzed by reverse transcription‑quantitative PCR following exposure to radiation. In addition, the levels of these proteins were measured by western blotting or ELISA. The results revealed that irradiation of mIMCD‑3 cells clearly triggered cellular senescence. Notably, Klotho gene expression was considerably decreased in radiation‑exposed mIMCD‑3 cells and in the kidney tissues of irradiated BALB/c mice, and the corresponding translated protein was consistently expressed following radiation exposure. Moreover, expression of TNF‑α, a negative regulator of Klotho, was significantly increased, whereas ADAM9/10/17, an ectodomain shedding enzyme of Klotho, was decreased in irradiated mIMCD‑3 cells and in the kidney tissues of BALB/c mice. Collectively, these data suggested that TNF‑α‑mediated inhibition of Klotho expression and blockage of soluble Klotho formation via decreased ADAM expression following irradiation may contribute to the development of renal dysfunction through acceleration of radiation‑induced cellular senescence.Sebaceous gland carcinoma (SGC) of the eyelid is an uncommon aggressive tumor with a relatively high rate of local recurrence and a poor prognosis following metastasis. However, the molecular mechanisms underlying the pathogenesis of SGC remain unclear. The purpose of the present study was to clarify microRNA (miRNA) expression profiles in SGC and to explore novel miRNA‑mRNA networks of SGC. A small RNA‑sequencing analysis was performed to identify miRNAs differentially expressed between SGC and sebaceous adenoma control samples. Bioinformatics analyses were conducted to reveal biological functions, canonical pathways and molecular interaction networks using integrated miRNA‑mRNA datasets, including mRNA expression profiles of SGC from our previous study. Selleckchem MGH-CP1 The present results demonstrated that 16 upregulated miRNAs and 516 downregulated mRNAs were associated with loss of lipid metabolism function and enriched in cholesterol biosynthesis pathways. By contrast, 29 downregulated miRNAs and 194 upregulated mRNAs were mainly associated with the promotion of cell survival and proliferation in addition to enrichment of DNA damage‑induced cell cycle‑regulation pathways. Furthermore, network analyses revealed that the upregulated miRNAs, miR‑130a‑3p and miR‑939‑5p, and the downregulated miRNAs, miR‑146a‑5p, miR‑149‑3p, miR‑193a‑3p, miR‑195‑5p and miR‑4671‑3p, could be upstream regulators related to these functional changes of SGC. These results improved the understanding of molecular mechanisms of SGC and may help to improve the diagnosis of SGC.Lung cancer is the most prevalent and observed type of cancer in Xuanwei County, Yunnan, South China. Lung cancer in this area is called Xuanwei lung cancer. However, its pathogenesis remains largely unknown. To date, a number of studies have shown that microRNA (miR)‑218 functions as a tumor suppressor in multiple types of cancer. However, the role of miR‑218 and its regulatory gene network in Xuanwei lung cancer have yet to be investigated. The current study identified that the expression levels of miR‑218 in XWLC‑05 cells were markedly lower compared with those in immortalized lung epithelial BEAS‑2B cells. The present study also demonstrated that overexpression of miR‑218 could decrease cell proliferation, invasion, viability and migration in Xuanwei lung cancer cell line XWLC‑05 and NSCLC cell line NCI‑H157. Additionally, the results revealed that overexpression of miR‑218 could induce XWLC‑05 and NCI‑H157 cell apoptosis by arresting the cell cycle at G2/M phase. Finally, the present study demonstrated that overexpression of miR‑218 could lead to a significant increase in phosphatase and tensin homolog ( in Xuanwei lung cancer. The results demonstrated that miR‑218 might serve a vital role in tumorigenesis and progression of Xuanwei lung cancer and overexpression of miR‑218 may be a novel approach for the treatment of Xuanwei lung cancer.The aim of the present study was to investigate the regulatory functions of microRNA (miR)‑26a‑5p on lipopolysaccharide (LPS)‑induced acute lung injury (ALI) and its molecular mechanisms. The role of miR‑26a‑5p on an ALI mouse model was evaluated by examining the histological changes, wet/dry (W/D) ratio, myeloperoxidase (MPO) activity, malondialdehyde (MDA) expression levels in lung tissues and the survival of ALI mice. Moreover, the protein concentration and the number of neutrophils and lymphocytes in bronchoalveolar lavage fluid (BALF) was analyzed. To explore the effect of miR‑26a‑5p on inflammatory responses and apoptosis, the expression levels of tumour necrosis factor‑α (TNF‑α), interleukin (IL)‑1β and IL‑6 and apoptosis were measured by ELISA, terminal deoxynucleotidyl transferase‑mediated dUTP nick end labelling staining and flow cytometry in BALF, A549 cells and lung tissues. B‑cell lymphoma‑2 (Bcl‑2), Bax and cleaved caspase‑3 in lung tissues were measured by western blotting and reverse transcription‑quantitative PCR.