Notes

Portrayal regarding The reproductive system Microbiota of Primiparous Cows During Earlier Postpartum Durations within the Reputation and Shortage of Endometritis.
874; p=0.002), NLR≤1.6 (OR, 1.596; 95% CI, 1.207-2.111; p=0.001) and PNI≤53.1 (OR, 1.511; 95% CI, 1.136-2.009; p=0.005) were independent factors that predicted recurrence. Conclusion The NLR, PLR and PNI have predictive value for TNM stage and recurrence in patients with PTC, but their predictive efficiency is limited. Caution should be used when considering clinical applications of inflammation-based scores. © 2020 Chen et al.Objective At present, little is known regarding the specific risk factors of ocular metastasis (OM) in elderly patients with lung cancer. This study aimed to find out the risk factors of ocular metastasis. Methods A total of 1615 elderly patients with lung cancer were recruited into this retrospective study between April 2001 and July 2016. These patients were divided into two groups, namely OM and non-ocular metastasis (NOM). Student's t-tests, nonparametric rank sum tests, and Chi-square tests were applied to describe whether there were significant differences between the OM group and NOM group. We compared a range of serum biomarkers between the two groups of patients, including alkaline phosphatase, calcium, hemoglobin, alpha-fetoprotein, carcinoembryonic antigen, CA-125, CA-199, CA-153, CA-724, cytokeratin-19 fragment (CYFRA21-1), TPSA and neuron specific enolase (NSE). We used binary logistic regression analysis to determine the risk factors and receiver operating curve (ROC) analyses to assess the diagnostic value for OM in CRC patients. Results The incidence of OM in elderly patients with lung cancer was 2.0%. Binary logistic regression indicated that CA-125, CA-153, and total prostate specific antigen (TPSA) were identified as independent risk factors of OM in patients with lung cancer (P less then 0.001, P less then 0.001, and P=0.003, respectively). The sensitivity and specificity of OM diagnosis were as follows CA-125, 81.25% and 81.57%; CA-153, 68.75% and 83.78%; and TPSA, 81.25% and 90.03%, respectively. Conclusion The serum concentrations of CA-125, CA-153, and TPSA have predictive value in the diagnosis of OM in elderly patients with lung cancer. © 2020 Ge et al.Background AOC1 is a copper-containing amine oxidase that is responsible for catalyzing the deamination of polyamines, which produces reactive oxygen species. Previous studies have demonstrated that polyamines are involved in the regulation of proliferation, migration, and apoptosis of cells. However, very little is known about the functions and regulatory mechanisms of AOC1 in tumors. Methods Based on GEPIA data, we found that AOC1 was significantly upregulated in human gastric cancer tissues. We knocked down AOC1 in human AGS and MKN45 cells using siRNA transfection, then utilized qRT-PCR assay and Western blot to verify the effectiveness of AOC1 knockdown in gastric cancer cells. Results Function analysis demonstrated that knockdown of AOC1 inhibited the proliferation, invasion, and migration of human gastric cancer cells. Flow cytometry detection suggested that AOC1 knockdown induced apoptosis in human gastric cancer cells. Mechanism investigation suggested that AOC1 knockdown increased the ratio of Bax/Bcl2 and induced activation of the caspase cascade. Furthermore, the AKT signaling pathway was inactivated when AOC1 was silenced, including downregulated phosphorylation level of AKT and expression of downstream effectors, Cyclin D1, and p70S6K. Finally, we found that knockdown of AOC1 inhibited the epithelial-mesenchymal transition (EMT) in human gastric cancer by increasing the expression of epithelial markers E-cadherin, as well as decreasing mesenchymal marker N-cadherin, SNAIL and Slug. Conclusion Our study suggests that AOC1 functions as an oncogene in human gastric cancer by activating the AKT signaling pathway and EMT process and maybe a target of 6-mercaptopurine, which provides new insight in the clinical use of AOC1 in gastric cancer therapy. Src inhibitor © 2020 Xu et al.Background To investigate the pathological risk of prostate cancer (PCa) according to the obesity and metabolic status of Chinese patients undergoing radical prostatectomy. Materials and Methods We performed a retrospective cross-sectional study of 1016 patients with PCa who underwent radical prostatectomy and whose metabolic status and body mass index were examined. Multivariate logistic regression analysis was performed to examine the relationship between different metabolic obesity phenotypes and the pathological outcomes of PCa. Results Among 1016 men, 551 (54.2%), 106 (10.4%), 238 (23.4%), and 121 (11.9%) were assigned to the metabolically healthy and normal weight (MHNW) group, metabolically abnormal but normal weight (MANW) group, metabolically healthy but overweight or obese (MHO) group, and metabolically abnormal and overweight or obese (MAO) group, respectively. Compared with the MHNW group, the MAO group had a significantly greater risk of a higher prostatectomy Gleason score [odds ratio (OR), 1.907; 95% confidence interval (95% CI), 1.144-3.182], pathological stage (OR, 1.606; 95% CI, 1.035-2.493), and seminal vesicle invasion (OR, 1.673; 95% CI, 1.041-2.687). In contrast, the ORs were not increased in the MHO or MANW group. In the context of normal weight, metabolic disorders were associated with lymph node involvement. The metabolic status and body mass index were not associated with extracapsular extension or surgical margins in any of the four groups. Conclusion The MAO phenotype is associated with aggressive PCa, including a higher prostatectomy Gleason score, pathological stage, and seminal vesicle invasion and might also be associated with disease progression. Obesity and metabolic disorders act synergistically to increase the pathological risk of PCa. © 2020 Liu et al.Introduction At present, drug resistance remains a major obstacle for breast cancer (BCa) patients who receive tamoxifen (TAM) chemotherapy. In this study, we aimed to investigate the functional role of long non-coding RNA BLACAT1 in the acquisition of TAM resistance in BCa. Methods TAM-resistant BCa cells were derived by exposure to 1 μM of TAM for 6 months. The expression levels of BLACAT1 and miR-503 were detected by RT-qPCR analysis. Chemosensitivity of BCa cells to TAM was measured by MTT assay. link2 Apoptosis of BCa cells was detected by flow cytometric analysis, and the expression levels of apoptosis-related proteins were detected by Western blot analysis. The direct binding relation between BLACAT1 and miR-503 was predicted by bioinformatics analysis and verified by dual-luciferase reporter assay. Results Our findings showed that BLACAT1 was significantly upregulated in TAM-resistant BCa cells (MCF-7/TR and T47D/TR), and BLACAT1 knockdown markedly reduced the TAM resistance in these cells. Importantly, we observed that BLACAT1 might function as a competing endogenous RNA of miR-503 in MCF-7/TR and T47D/TR cells, thereby increasing the expression of oncogenic Bcl-2 protein. Rescue experiments showed that miR-503 inhibition partly blocked the inhibitory effect of BLACAT1 knockdown on TAM resistance of MCF-7/TR and T47D/TR cells. Conclusion To conclude, this study revealed that overexpressed BLACAT1 induces TAM resistance in human BCa partly by regulating miR-503/Bcl-2 axis, potentially benefiting BCa treatment in the future. © 2020 Qu et al.Purpose Phosphoinositide 3-kinase (PI3K) and the downstream Akt/mammalian target of rapamycin (mTOR) pathway are central to the control of cell proliferation and survival. Although abnormal activation of this pathway has been well established in a variety of tumours, limited studies are available on synovial sarcoma. The aim of this study was to investigate the expression of several key proteins of those pathways in synovial sarcomas and to correlate the expression of these proteins with clinicopathologic features and prognosis. Patients and Methods A total of 174 patients with synovial sarcomas were recruited for this study. The phosphorylation status of Akt, mTOR, and eukaryotic translation initiation factor 4E binding protein (4E-BP1) was measured by immunohistochemistry assays in formalin-fixed, paraffin-embedded samples. Correlations between the expression levels of these proteins and clinicopathologic features and prognosis were analysed. Results The positive rates of phosphorylated (p)Akt, pmTOR, p4E-Bhe high expression of pAkt, pmTOR, and p4E-BP1 associated with aggressive clinical behaviour in synovial sarcomas and provided evidence for prognostic evaluation and targeted therapy. link3 © 2020 Li et al.Background lncRNA-SNHG16 was identified as an oncogene in many cancers, but its involvement in prostate carcinoma is unknown. Material and Method Expression of lncRNA-SNHG16 and glucose transporter 1 (GLUT-1) in 52 prostate carcinoma tissues and 36 normal prostate tissues was analyzed by RT-qPCR. Transfections were performed to analyze gene interactions. Cell proliferation was analyzed by cell proliferation assay. Results Overexpression of lncRNA-SNHG16 effectively distinguished prostate carcinoma patients from normal ones. Expression levels of lncRNA-SNHG16 and GLUT-1 mRNA were significantly and positively correlated across prostate carcinoma tissues. In vitro cancer cell experiments revealed that lncRNA-SNHG16 siRNA silencing downregulated the expressions of GLUT-1 and reduced glucose uptake. lncRNA-SNHG16 siRNA silencing also significantly inhibited prostate carcinoma cell proliferation. However, lncRNA-SNHG16 siRNA silencing did not affect the normal prostate. Conclusion In conclusion, lncRNA-SNHG16 might be a possible treatment target for prostate cancer. © 2020 Shao et al.Background Prostate cancer (PC) is one of the most common carcinomas in men worldwide. The lack of effective therapies urges the development of novel therapeutic options against PC. Quercetin (Quer) is a flavonoid compound that has been shown to effectively inhibit PC in vitro and in vivo. However, the underlying mechanisms await elucidation. Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC. Previous data showed that quercetin promoted the apoptosis of fibroblast-like synoviocytes by upregulating MALAT1 in rheumatoid arthritis. However, we speculate that mechanisms are different in PC. Materials and Methods Human PC cell line PC-3 and its xenograft tumor were chosen as in vitro and in vivo models for PC. A series of in vitro and in vivo functional experiments were carried out to elucidate the role of MALAT1 in quercetin treatment against PC. Western blot was performed to measure the expression of related proteins to explore underlying molecular mechanisms. Results We showed for the first time that MALAT1 expression was significantly downregulated in quercetin-treated PC cells in a dose- and time-dependent manner. Also, quercetin inhibited the proliferation of PC cells and the growth of xenograft tumors. Moreover, quercetin suppressed EMT process, promoted apoptosis and deactivated PI3K/Akt signaling pathway during the progression of PC. MALAT1 overexpression in PC cells resulted in the resistance against quercetin treatment. Conclusion Our study illustrated, for the first time, that MALAT1 played an important role in quercetin treatment against PC by inhibiting EMT process and promoting apoptosis, providing a new molecular basis for the application of quercetin in PC treatment. © 2020 Lu et al.
Website: https://www.selleckchem.com/products/Dasatinib.html