Churchillholme2491

Gain-of-function of miR-574-3p downregulated the expression levels of ADAM28 in liver cancer cells. Additionally, overexpression of ADAM28 significantly attenuated the suppressive effect of miR-574-3p on the growth of liver cancer cells. The present results provide novel insights into the function of the miR-574-3p/ADAM28 signaling pathway in liver cancer.Interleukin-21 (IL-21) is an important cytokine that is currently being investigated for its potential use in tumor immunotherapy in the future. In tumor cells, IL-21 stimulates the immune response by increasing the cytotoxic activity of natural killer cells, B cells and CD8+ T cells, which in turn induces the apoptosis of tumor cells. The therapeutic effects of IL-21 have been investigated in several types of disease and numerous clinical trials are in progress. The aim of the present study was to determine the role of IL-21 in oral squamous cell carcinoma (OSCC) in vitro. IL-21 expression was detected in OSCC tissues via RT-qPCR, western blotting and immunohistochemistry analyses. The results demonstrated that IL-21 protein expression decreased in OSCC tissues. IL-21 was overexpressed using adenovirus in CAL-27 cells. The Cell Counting Kit-8 assay demonstrated that overexpression of IL-21 inhibited cell proliferation. Furthermore, overexpression of IL-21 inhibited cell migration, detected by the wound healing assay, and promoted cell apoptosis, detected by TUNEL staining and flow cytometry analysis. The results demonstrated that overexpression of IL-21 inhibited activation of the JNK signaling pathway. In conclusion, the findings of the present study suggest that IL-21 may function as a potent antitumor agent in OSCC.Enzalutamide, an androgen receptor inhibitor, has been clinically approved for the treatment of metastatic castration-resistant prostate cancer (CRPC) in the United States. However, patients only benefit from enzalutamide for a short period of time as resistance may develop. Therefore, it is vital to develop a novel strategy to overcome enzalutamide resistance. Ras-related C3 botulinum toxin substrate 1 (Rac1), which is commonly upregulated in human cancer types, has been recognized as a key molecular component in tumorigenesis, invasion and metastasis. However, the role of Rac1 in enzalutamide-resistance in prostate cancer (PCa) remains unknown. In the present study, Rac1 was demonstrated to be upregulated in enzalutamide-resistant PCa cells, and Rac1 knockdown inhibited enzalutamide-resistant cell proliferation and colony formation. Western blotting results indicated that enzalutamide treatment downregulated the expression levels of JNK and activated transcription factor 2, as well as enhanced the Bax/Bcl-2 ratio and induced cleavage of poly-ADP ribose polymerase. Moreover, knockdown of Rac1 in MR49F cells significantly inhibited cell migration and invasion via the downregulation of Snail and the upregulation of E-cadherin. The results of a nude mouse xenograft tumor model using 22RV1 cells demonstrated that enzalutamide inhibited tumor growth after Rac1 knockdown dramatically, compared to vehicle and single treatment groups. Therefore, the present study provided novel evidence that Rac1 may serve a crucial role in enzalutamide resistance, and that targeting Rac1 may be a potential approach for the treatment of CRPC.In the present study, the predictive role of the percentage of the solid portion volume (PSV) in patients with lung adenocarcinoma was investigated. The PSV was obtained through quantitative volumetric assessments based on reconstructed CT images of lung adenocarcinoma by comparing the index among tumors with c-ros oncogene 1 (ROS1) rearrangement, epidermal growth factor receptor (EGFR) mutations, echinoderm anaplastic lymphoma kinase (ALK) rearrangements or wild-type (WT) status for the three genes. Among 1,120 patients with lung adenocarcinoma, 28 patients with ROS1 rearrangement lung adenocarcinoma, 71 with ALK rearrangement and 578 with EGFR mutations were diagnosed. PSV was quantitatively measured by semi-automated nodule assessment software and compared in patients with different mutation statuses. The PSV (presented as the median with interquartile range) in the ROS1 rearrangement group [87.9 (82.7-92.3)%] was higher than that in the EGFR mutation group [70.4 (51.4-83.4%)] and the WT group [63.0 (50.9-83.2)%; P less then 0.001], but was similar to that in the ALK rearrangement group [84.0 (70.3-90.0)%; P=0.251]. The area under the receiver operating characteristic curve (AUC) for the PSV to predict ROS1 or ALK rearrangement combined was 0.702 (95% CI 0.631-0.773; P less then 0.001); at a cut-off value of 0.805 (when the Youden index was maximal), the predictive sensitivity was 0.697 and the specificity was 0.702. Younger age and higher PSV values were independent predictors of ROS1/ALK rearrangements. The AUC for the predictive model combined with age and PSV was 0.785. In conclusion, the PSV in the lung adenocarcinomas with ROS1 rearrangement was significantly higher compared with that in the EGFR-mutated and WT lung adenocarcinoma, but was similar to that in lung adenocarcinoma with ALK rearrangement. read more Younger age and higher PSV values on CT in patients with lung adenocarcinomas were predictive factors for ROS1/ALK rearrangement.The effect of nivolumab and the relation between bone response and tumor control in patients with non-small-cell lung cancer (NSCLC) with bone metastases are not clear. The outcome of nivolumab monotherapy was investigated, and whether the response of bone metastases is useful as an early predictor of tumor control in patients with NSCLC with bone metastases was examined. The participants included 15 patients who received nivolumab monotherapy for NSCLC with bone metastases in our institution between 2015 and 2017. Tumor control was defined using Response Evaluation Criteria in Solid Tumors, version 1.1 (RECIST1.1). Response of bone metastases was assessed by the MD Anderson response criteria (MDA criteria). Responses according to RECIST1.1 and the MDA criteria were classified as responder (complete response or partial response) and non-responder [progressive disease (PD) or stable disease]. Progression-free survival (PFS) was investigated using the Kaplan-Meier method. With RECIST1.1, the overall response rate was 20%.