Contrerascunningham8280

Importantly, the effects of SAL were impaired upon the silencing of miR‑133a, whereas the overexpression of miR‑133a partly restored the effects of SAL. On the whole, the findings of the present study demonstrate that SAL inhibits the ox‑LDL‑induced upregulation of miR‑133a expression, while promoting the expression of Bcl‑xL, thereby preventing endothelial cell apoptosis.Leukemia is a type of cancer which originates in blood‑forming tissues. MicroRNAs (miRNAs or miRs) have been shown to be involved leukemogenesis. In the present study, following the gain‑ and loss‑function of miR‑145 and ATP‑binding cassette sub‑family E member 1 (ABCE1) in K562 cells and K562 adriamycin‑resistant cells (K562/ADM cells), the levels of multidrug resistance protein 1 (MRP1) and P‑glycoprotein (P‑gp) were measured. The viability of the K562 cells and K562/ADM cells treated with various concentrations of ADM, and cell sensitivity to ADM were measured. The apoptosis of stem cells was detected. selleckchem K562/ADM cells were transfected with miR‑145 mimic or with miR‑145 mimic together with ABCE1 overexpression plasmid to examine the effects of ABCE1 on the sensitivity of K562/ADM cells to ADM. The association between miR‑145 and ABCE1/MRP1 was then verified. The dose‑ and time‑dependent effects of ADM on the K562 cells and K562/ADM cells were examined. The K562/ADM cells exhibited a greater resistance to ADM, higher levels of MRP1 and P‑gp, and a lower miR‑145 expression. The K562/ADM cells and stem cells in which miR‑145 was overexpressed exhibited a suppressed cell proliferation, decreased MRP1 and P‑gp levels, and an increased apoptotic rate. However, K562 cells with a low expression of miR‑145 exhibited an increased cell proliferation, increased levels of MRP1 and P‑gp, and a suppressed apoptotic rate. Compared with the overexpression of miR‑145, the combination of miR‑145 and ABCE1 decreased the sensitivity of drug‑resistant K562/ADM cells to ADM. The above‑mentioned effects of miR‑145 were achieved by targeting ABCE1. Taken together, the findings of the present study demonstrate that the overexpression of miR‑145 promotes leukemic stem cell apoptosis and enhances the sensitivity of K562/ADM cells to ADM by inhibiting ABCE1.Breast cancer is one of the most prevalent cancer types and is accompanied by a high incidence and mortality rate, severely threatening women's health globally. Long non‑coding RNA forkhead box D2 adjacent apposite strand RNA 1 (lncRNA FOXD2‑AS1) has been identified to function as an oncogene in human cancers; however, it has rarely been investigated in breast cancer. The aim of the present study was to investigate the role of FOXD2‑AS1 in breast cancer, and to clarify the underlying mechanisms. The expression of FOXD2‑AS1 in breast cancer cell lines was first quantified by reverse transcription‑quantitative PCR, and the biological function of FOXD2‑AS1 was then determined. Cellular proliferative ability was determined by Cell Counting kit‑8 assay, and wound healing and Transwell assays were conducted to assess the cell migratory and invasive ability. Corresponding protein expression levels were determined by western blot analysis. In addition, experimental animal models were established by the subcutaneous ited protein signaling. On the whole, the findings of the present study suggest that the FOXD2‑AS1/S100A1/Hippo axis is involved in the tumorigenesis and progression of breast cancer. In the future, these may contribution to the identification of more effective breast cancer treatments.MicroRNAs (miRNAs) have been reported to have important regulatory roles in the progression of several types of cancer, including cervical cancer (CC). However, the biological roles and regulatory mechanisms of miRNAs in CC remain to be fully elucidated. The aim of the present study was to examine the functions of miRNAs in CC and the possible mechanisms. Using a microarray, it was identified that miRNA‑15a‑5p (miR‑15a‑5p) was one of the most downregulated miRNAs in CC tissues compared with adjacent noncancerous tissues. The low expression of miR‑15a‑5p was observed in CC tumor tissues with distant metastasis and in CC cell lines. In addition, the effects of miR‑15a‑5p upregulation on cell viability, apoptosis, invasion and migration of CC cells were investigated using CCK‑8, flow cytometry, Transwell and wound healing assays, respectively. It was demonstrated that upregulation of miR‑15a‑5p significantly suppressed the viability, migration and invasion, and promoted the apoptosis of SiHa and C‑33A cells. Furthermore, yes‑associated protein 1 (YAP1), a well‑known oncogene, was confirmed to be directly targeted by miR‑15a‑5p and was found to be negatively regulated by miR‑15a‑5p. Further correlation analysis indicated that miR‑15a‑5p expression was negatively correlated with YAP1 expression in CC tissues. Notably, overexpression of YAP1 abrogated the tumor suppressive effects of miR‑15a‑5p in CC cells. Taken together, these present findings indicated that the miR‑15a‑5p/YAP1 axis may provide a novel strategy for the clinical treatment of CC.The outbreak of the 2019 coronavirus disease (named, COVID‑19), caused by the novel SARS‑CoV‑2 virus, represents a worldwide severe threat to public health. It is of the utmost importance to characterize the immune responses against the SARS‑CoV‑2 and the mechanisms of hyperinflammation, in order to design better therapeutic strategies for COVID‑19. In the present study, a transcriptomic analysis was performed to profile the immune signatures in lung and the bronchoalveolar lavage fluid samples from COVID‑19 patients and controls. Our data concordantly revealed increased humoral responses to infection. The elucidation of the host responses to SARS‑CoV‑2 infection may further improve our understanding of COVID‑19 pathogenesis and suggest better therapeutic strategies.Angiogenesis and vascular maturation play important roles in tumorigenesis and tumor development. The expression of neuropilin 1 (NRP1) is closely associated with angiogenesis in tumors; however, the molecular mechanisms of action in angiogenesis and tumor maturation, as well as the potential clinical value of NRP1 remain unclear. The importance of NRP1 expression in tumor progression was determined using The Cancer Genome Atlas (TCGA) database analysis. Gain‑ and loss‑of‑function experiments of NRP1 were performed in vascular endothelial cells (ECs) to investigate the functions in angiogenesis. CCK‑8, flow cytometry, Transwell experiments and a series of in vitro experiments were used to detect cell functions. A combination of angiogenesis antibody arrays and RNA‑Seq analyses were performed to reveal the proangiogenic mechanisms of action. The function of semaphorin 4D (SEMA4D) was also investigated separately. NRP1 mRNA levels were significantly increased in primary tumors compared with normal tissues based on TCGA data (P less then 0.