Mechanobiology of the feminine the reproductive system

the expression levels of ATP7A and ATP7B, which are important proteins in the tumorigenesis and chemotherapy of lung adenocarcinoma. The present study provided evidence for the potential use of Salvia miltiorrhiza extract for treating lung adenocarcinomas in the clinic.An increasing body of evidence indicates the involvement of microRNAs (miRNAs/miRs) in the initiation and progression of colorectal cancer (CRC). miR-296-5p was recently identified as a tumor suppressor in a variety of human cancer types; however, its function in CRC remains largely unknown. The present study demonstrated that the expression of miR-296-5p was significantly downregulated in CRC tissues and cell lines. The overexpression of miR-296-5p markedly inhibited proliferation, and induced cell cycle arrest and apoptosis in CRC cells. Bioinformatics analysis suggested that high mobility group AT-hook 1 (HMGA1) may be a target of miR-296-5p in CRC cells. Further experiments showed that miR-296-5p bound the 3'-untranslated region of HMGA1 and decreased its expression in CRC cells. HMGA1 was overexpressed in CRC tissues and was inversely correlated with the expression of miR-296-5p. The restoration of HMGA1 significantly reversed the inhibitory effect of miR-296-5p on the proliferation of CRC cells. Overall, the findings of the present study indicate that miR-296-5p suppressed the progression of CRC, at least partially via targeting HMGA1. Thus, miR-296-5p is a potential target for novel therapies in CRC.Triple-negative breast cancer (TNBC) is highly invasive, has a high rate of recurrence and is associated with a poor clinical outcome when compared with non-TNBC due to a lack of effective and targeted treatments. The coatomer protein complex subunit β2 (COPB2) is upregulated in various types of malignant cancer. The present study demonstrated that COPB2 expression levels were significantly upregulated in breast carcinoma HS-578T cells (clonal cells originating from TNBC) when compared with non-TNBC MCF-7 cells. HS-578T cells also exhibited higher rates of proliferation, invasion and transendothelial migration when compared with MCF-7 cells. Moreover, it was identified that genetically silencing the COPB2 gene using a lentivirus-short hairpin RNA inhibited the proliferative, colony formation, migratory and invasive properties of the TNBC HS-578T cells. Mediation of the COPB2 silencing effect may be associated with regulating the phosphorylation of serine/threonine kinase AKT in the PI3K/AKT signaling pathway. These results suggested the importance of COPB2 in promoting the proliferation of TNBC cells and identified COPB2 as a potential novel therapeutic target.Excessive proliferation and migration of vascular smooth muscle cells (VSMCs) is the main cause of arteriosclerosis obliterans (ASO). The present study aimed to investigate the role of microRNA (miR)-125b on the proliferation and migration of VSMCs. BVD-523 Platelet-derived growth factor-BB (PDGF-BB; 20 ng/ml) was used to treat VSMCs to establish an in vitro model of ASO. VSMCs were transfected with miR-125b mimic to overexpress miR-125. Cell Counting kit-8 (CCK-8) and BrdU assays were performed to assess the proliferative ability of VSMCs, while Transwell and wound healing assays were performed to assess the migratory ability of VSMCs. Western blot and immunofluorescence analyses were performed to detect the expression levels of angio-associated migratory cell protein (AAMP) and serum response factor (SRF) in VSMCs following transfection with miR-125b mimic or inhibitor. The results demonstrated that miR-125b expression decreased following treatment with PDGF-BB, the effects of which were reversed following transfection with miR-125b mimic. According to the CCK-8 assay, the cell proliferative ability decreased by ~50% compared with the negative control (NC) group, and ~40% at day 4 based on the BrdU assay. The results of the Transwell and wound healing assays indicated that the migratory ability of VSMCs significantly decreased in the miR-125b mimic group compared with the NC group. Furthermore, western blot and immunofluorescence analyses demonstrated that AAMP and SRF expression levels decreased following transfection with miR-125b mimic compared with the NC group, the effects of which were reversed following transfection with miR-125 inhibitor. Taken together, the results of the present study suggested that miR-125b inhibits the proliferative and migratory abilities of VSMCs by regulating the expression levels of AAMP and SRF.
The prediction of the individual's response to disease modifying antirheumatic drugs (DMARDs) in rheumatoid arthritis (RA) is challenging and often limited. Here we evaluated the influence of patients' expectations towards a change in treatment with DMARD on clinical outcome in RA.
One hundred patients (74 female) with RA (2010 ACR/EULAR classification criteria) and an upcoming change in DMARD treatment due to non-response or adverse effects were included. Patients' treatment beliefs, health-related quality of life and treatment expectations were measured using the Beliefs about Medicines Questionnaire (BMQ), the Short Form 36, and self-designed questions about expectations before treatment initiation (T0), and DAS28-CRP was calculated at T0 and after 4 months (T4). Associations between patients' beliefs and expectations and changes in DAS28-CRP (T0 to T4, ΔDAS28-CRP) were explored by regression analyses after multiple imputation.
A total of 99 patients were included, of whom 84 completed all questionnaires. Thirty-six percent of all variability in treatment response (ΔDAS28-CRP) was explained by expectations assessed with the questionnaires and the C-reactive protein (CRP)-value at T0. Among these, the expected improvement rate, with 10.5%, as well as the CRP-value at T0, with 10.6%, had the greatest positive effect whereas the fear of adverse effects, with 11.4%, and the BMQ.concern scale, with 9.0%, had the greatest negative impact on ΔDAS28.
Patients' expectations towards newly induced DMARD therapies influence clinical response and may serve as possible explanatory factors for treatment response affecting subjective and objective outcome parameters.
DRKS00017005.
DRKS00017005.