Livingstonmygind6482

The miR-187-triggered growth inhibition was found to be mainly due to induction of G2/M phase cell cycle arrest of the SAOS-2 cells. The G2/M cell cycle arrest was also accompanied by depletion of Cyclin-B1 expression. Additionally, miR-187 enhanced the chemosensitivity of the osteosarcoma cells to doxorubicin. The wound healing and transwell assay showed that miR-187 overexpression resulted in the suppression of migration and invasion of the SAOS-2 osteosarcoma cells. In silico analysis showed that miR-187 exerts its effects by inhibiting mitogen activated protein kinase 7 (MAPK7). The expression of MAPK7 was found to be significantly upregulated in osteosarcoma cells and overexpression of MAPK7 could nullify the effects of miR-187 on the proliferation of the osteosarcoma cells.PURPOSE Myxofibrosarcoma is characterized by a high rate of recurrence after surgery. Since myxofibrosarcoma is refractory to conventional cytotoxic chemotherapy, the established radical treatment is primary wide resection. The effects of histone deacetylase (HDAC) inhibitors on myxofibrosarcoma have not yet been investigated. Therefore, the main purpose of the present study was to examine the effects of a HDAC inhibitor on myxofibrosarcoma. METHODS The effects of the HDAC inhibitor OBP-801 on human myxofibrosarcoma cells were examined using cell viability assay, flow cytometric analysis of the cell cycle and apoptosis, and Western blotting. The effects of combinations of OBP-801 with pazopanib or Akt-mTOR inhibitors were also investigated using cell viability assay. RESULTS OBP-801 inhibited the growth of myxofibrosarcoma NMFH-1 and NMFH-2 cells. It also induced cell cycle arrest at the G2 phase and apoptosis in both cell lines. The inhibitory effects of pazopanib and Akt-mTOR inhibitors on the growth of myxofibrosarcoma cells were enhanced by the combination with OBP-801. CONCLUSIONS The present results demonstrated that OBP-801 exerted therapeutic effects in myxofibrosarcoma in both single and concomitant administrations. Therefore, OBP-801 has potential as a novel treatment for myxofibrosarcoma.PURPOSE This is a prospective pair cohort validating study to assess the clinical performance of a 3D ultrasound-guided imaging device (HistoScanning) to detect clinically significant prostate cancer. METHODS Data was collected prospectively from April 2016 to September 2018 from 200 patients who had their serum PSA levels rising for at least 4 months after previous negative trans rectal ultrasound-guided TRUS biopsy in a single center. All eligible men underwent prostate HistoScanning (PHS) and transperineal template prostate mapping biopsy as our reference standard and additional single targeted biopsy, when PHS device tested positive with a suspicious lesion of ≥0.5 cm3. Our primary goal was to obtain the results of PHS ability to detect clinically significant prostate cancer. Our secondary goal was to acquire data on PHS targeted biopsies. RESULTS In our study 200 men were enrolled and their mean age was 62 ±5.9 years. The mean number of previous biopsies was 1.51±0.65. The mean volume for PHS index lesion in any one prostate was 1.56 ±2.01 ml. Clinically significant prostate cancer (csPCa) was detected in 41 (20.5%) patients on biopsy. Sensitivity of PHS for detecting csPCa was 61.9% (95% CI 45.64-76.43) with specificity 27.85% (95% CI 21-35.53). Positive predictive value (PPV) and negative predictive value (NPV) for PHS were 18.57% (95% CI 15-22.76) and 73.33% (95% CI 63.45-81.33), respectively. Overall accuracy calculated by AUROC curve was 0.39 (95% CI 0.3-0.47). selleck chemicals CONCLUSION PHS performance results of our study on detecting clinically significant prostate cancer were insufficient to include this ultrasound-guided diagnostic test as standard diagnostic tool.PURPOSE Prostate cancer is considered to be one of the most common cancers in men and as such there is a pressing need for finding new therapeutic agents to treat this disease. Therefore, the main purpose of the current research work was to study the anticancer effects of a naturally occurring coumarin- Auraptenol- against drug-resistant human prostate cancer cells and evaluate its effects on programmed cell death, reactive oxygen species (ROS) production, and JNK/p38 MAPK signalling pathway. METHODS Cell proliferation was examined by CCK8 cell viability assay. Apoptosis-related studies were checked by fluorescent microscopy using acridine orange (AO)/ethidium bromide (EB) and Hoechst staining, as well as flow cytometry using annexin V/propidium iodide (PI) assay. Western blot was used to study the effects of Auraptenol on apoptosis-related protein expressions including Bax, Bcl-2, as well as JNK/p38 MAPK signalling pathway. ROS production was evaluated by flow cytometry. RESULTS The results showed that Auraptenol caused significant reduction in the viability of the human LNCaP prostate carcinoma cells in a dose-dependent manner, exhibiting an IC50 of 25 µM in cancer cells and IC50 of 100 µM in normal PNT2 cells. The AO/EB staining assay showed that Auraptenol inhibited the viability of cancer cells via induction of apoptotic cell death, which was associated with increase in Bax and decrease in Bcl-2 levels. Hoechst staining results also confirmed that Auraptenol induced programmed cell death. The apoptotic cells increased from 0.8% in the control to 32.5% in the study group at 50 µM concentration of Auraptenol. Auraptenol also induced an increase in ROS production in a dose-dependent manner. Finally, this molecule blocked the JNK/p38 MAPK signal pathway concentration-dependently in human prostate cancer cells. CONCLUSION In conclusion, the current study indicates that this molecule could be developed as a potential anticancer drug against human prostate carcinoma provided further studies are carried out.PURPOSE To explore the relationships of pain in pancreatic cancer patients with pathological stage and expressions of nuclear factor-κB (NF-κB) and cyclooxygenase-2 (COX-2). METHODS A total of 54 patients with pancreatic cancer were enrolled to evaluate the pain before treatment, detect the expressions of NF-κB and COX-2, an inflammatory mediator, in tumor tissues by the immunohistochemical method and analyze their relationships with the pain in these patients. RESULTS The expressions of NF-κB and COX-2 varied obviously among pancreatic cancer patients with different degrees of pain, and as the pain was aggravated, the patients had raised expressions of NF-κB and COX-2 in tumor tissues (p less then 0.05). The degree of pain also differed evidently among the patients at different tumor node metastasis (TNM) stages, and the higher the pathological stage, the higher the degree of pain in patients (p less then 0.05). The pain score of patients was positively correlated with the expressions of NF-κB and COX-2 (p less then 0.