Rosafrandsen6027

A dual luciferase reporter assay indicated that insulin-like growth factor (IGF)-1 was a target gene of miR-130a-3p. Pearson's correlation analysis revealed a negative correlation between serum IGF-1 and serum exosomal miR-130a-3p levels. More importantly, exosomes from patients with DTC increased the expression of IGF-1 and p-PI3K/p-AKT, but these effects were abolished by siRNA targeting IGF-1 in TPC-1 cells. Taken together, the findings of the present study indicated that reduced exosomal miR-130a-3p levels were associated with the risk of DTC and may be used as a biomarker for the diagnosis of DTC.Lung adenocarcinoma (LUAD) has been considered as the most common cause of cancer-associated mortality. Radiotherapy resistance is one of the main reasons for LUAD treatment failure. The microRNA (miR)-101-3p has been previously reported to function as a tumor suppressor in several types of cancer, including LUAD. The present study aimed to explore the role and mechanism of miR-101-3p on radioresistance of lung adenocarcinoma cells through bioinformatics analysis and biological experiments. Based on the analysis of Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) data, it was demonstrated that the expression of miR-101-3p was low in LUAD tissues compared with normal lung tissues and was associated with poor prognosis of patients with LUAD. The results of the CCK-8 assay, colony formation assay, immunofluorescence staining, caspase-3 activity assay and western blotting demonstrated that miR-101-3p overexpression sensitized LUAD cells to ionizing radiation by decreasing the abilities of LUAD cell proliferation, colony formation, DNA damage repair and increasing caspase-3 activity and apoptosis of LUAD cells following ionizing radiation. Furthermore, according to bioinformatics analysis and luciferase assay, baculoviral IAP repeat containing 5 (BIRC5) was identified as a direct target of miR-101-3p. Increased BIRC5 expression reversed the miR-101-3p-mediated increase in LUAD cell radiotherapy sensitivity. Taken together, the results of the present study demonstrated that miR-101-3p may be considered as a potential target that can enhance LUAD cell sensitivity to radiotherapy, which may provide a new strategy to improve therapy in patients with LUAD.The initial diagnostic distinction between benign and malignant soft tissue tumors is critical for decisions regarding the appropriate course of treatment. The current study aimed to evaluate the vascularity and elasticity of soft tissue tumors by superb microvascular imaging and shear wave elastography using ultrasonography (US), to determine their usefulness in distinguishing malignant soft tissue tumors, and to further establish the diagnostic accuracy and usefulness of a scoring system (SS) based on these evaluations. The present study used 167 lesions of soft tissue tumors examined by US prior to biopsy, surgery and pathological tissue diagnosis. The vascularity index (VI) and the maximal shear velocity (MSV), as indices of vascularity and elasticity respectively, were evaluated using US. The tumor size and depth were also evaluated via magnetic resonance imaging (MRI). Based on the odds ratio of these parameters determined by multivariate logistic regression analysis, an original SS was established to identify the malignancy of soft tissue tumors. VI and MSV exhibited significantly high values for malignant tumors. Tumor size was also significantly larger for malignant than benign tumors. The areas under the curves (AUCs) of the receiver operating characteristic analysis for VI, MSV and tumor size were 0.75, 0.84 and 0.69, respectively, indicating that these methods were effective for the diagnosis of malignancy. An original SS consisting of VI, MSV and tumor size, excluding tumor depth, was established, and revealed an AUC value of 0.90, with 93.6% sensitivity and 79.2% specificity for malignancy distinction. US evaluation of vascularity and elasticity was an effective technique to distinguish malignant soft tissue tumors, and the current SS based on US evaluations including tumor size via MRI demonstrated a high diagnostic accuracy for malignant soft tissue tumors.Epstein-Barr virus (EBV) mainly causes infectious mononucleosis and is associated with several neoplasms, including Burkitt's lymphoma, nasopharyngeal carcinoma and lymphoproliferative disease. Human telomerase reverse transcriptase (hTERT) regulates enzymatic activity of telomerase and is closely associated with tumorigenesis and senescence evasion. Triptolide (TP) is a diterpenoid triepoxide, with a broad-spectrum anticancer and immunosuppressive bioactivity profile. The present study investigated whether TP inhibited hTERT expression and suppressed its activity. The mRNA and protein levels of hTERT were examined by reverse transcription-quantitative PCR and western blotting. The activity of hTERT promoter was determined by dual-luciferase reporter assay. Cell Counting Kit-8 assays were performed to analyze cell proliferation. The present study used EBV-positive B lymphoma cells as a model system, and the results demonstrated that TP significantly decreased hTERT transcription and protein expression. Mechanistically, TP attenuated the hTERT promoter activity by downregulating the expression levels of specificityprotein 1 and c-Myc transcription factors. Consistently, inhibition of hTERT via shRNA transfection efficiently enhanced the suppression of cell proliferation by TP. Furthermore, TP increased virus latent replication and promoted the lytic cycle of EBV in EBV-positive B lymphoma cells, increasing the number of lytic cells and inhibiting the viability of tumor cells. find more Taken together, the results of the present study revealed a molecular mechanism of the pharmacological inhibition of tumor cell proliferation by TP, encouraging the translation of TP-based therapeutics in EBV-positive B lymphoma treatment.Hepatocellular carcinoma (HCC) has an increasing incidence worldwide, and the global 5-year survival rate ranges from 5-30%. In China, HCC seriously threatens the nation's health; the incidence of HCC ranks fourth among all theriomas, and the mortality rate is the third highest worldwide. The main therapies for HCC are surgical treatment or liver transplantation; however, most patients with HCC will experience postoperative recurrence or metastasis, eventually resulting in mortality. As for advanced or unresectable HCC, the current appropriate treatment strategy is transarterial chemoembolization; however, limited therapeutic effect and natural or acquired drug resistance affect the efficacy of this approach. Previous studies have demonstrated that PD-L1 expression on host cells and myeloid cells plays an important role in PD-L1 blocked-mediated tumor regression. Thus, further research on programmed cell death protein 1 (PD-1) and programmed death-ligand 1 (PD-L1) is required. Countries including the United States, France, Britain and China have developed PD-1/PD-L1 blockers, including nivolumab, pembrolizumab, cemiplimab, atezolizumab, avelumab, durvalumab, toripalimab, sintilimab and camrelizumab.