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Tumor suppressor candidate 3 (TUSC3) is a coding gene responsible for N-glycosylation of many critical proteins. TUSC3 gene plays an oncogenic role in colorectal cancer (CRC), however, the role of TUSC3 in drug resistance of CRC is still unclear. The aim of this study is to investigate the biological function and molecular mechanism of TUSC3 in CRC drug resistance. The expression of TUSC3 in CRC is positively correlated to tumor stage in 90 paired clinical samples, and negatively associated with overall survival and disease-free survival of CRC patients. In vitro, TUSC3 promotes the formation of stemness and induces the drug resistance to 5-fluorouracil (5-FU) and cis-Dichlorodiammineplatinum(II) (DDP) in CRC cells. The tissue microarray assay and bioinformatic analysis indicates that TUSC3 may promote the expression of CD133 and ABCC1 via hedgehog signaling pathway. Treatment of Hedgehog signaling pathway agonist or inhibitor in TUSC3-silenced or TUSC3-overexpressed cells reverse the effects of TUSC3 in cellular stemness phenotype and drug resistance. Meanwhile, co-immunoprecipitation and immunofluorescence assays indicate a tight relationship between TUSC3 and SMO protein. Our data suggests that TUSC3 promotes the formation of cellular stemness and induces drug resistance via Hedgehog signaling pathway in CRC. © The Author(s) 2020. Published by Oxford University Press. All rights reserved. For Permissions, please email [email protected] features and the ecology of suitable hosts influence the phenology of invasive tick species. The southern cattle fever tick, Rhipicephalus (Boophilus) microplus (Canestrini) (Ixodida Ixodidae), vectors causal agents of babesiosis in cattle and it infests exotic, feral nilgai, Bosephalus tragocamelus Pallas, and indigenous white-tailed deer, Odocoilus virginianus (Zimmerman), on the South Texas coastal plain wildlife corridor. The corridor extends from the Mexico border to cattle ranches extending north from inside Willacy Co. Outbreaks of R. microplus infesting cattle and nondomesticated ungulate hosts since 2014 in the wildlife corridor have focused attention on host infestation management and, by extension, dispersal. However, there is a knowledge gap on the ecology of R. microplus outbreaks in the South Texas coastal plain wildlife corridor. Ixodid distribution on the wildlife corridor is strongly influenced by habitat salinity. Saline habitats, which constitute ≈25% of the wildlife corridor, harbor few ixodids because of occasional salt toxicity from hypersaline wind tides and infrequent storm surges, and from efficient egg predation by mud flat fiddler crabs, Uca rapax (Smith). Rhipicephalus microplus infestations on nilgai were more prevalent in part of the corridor with mixed low salinity and saline areas than in an area that is more extensively saline. The different levels of R. microplus infestation suggest that man-made barriers have created isolated areas where the ecology of R. microplus outbreaks involve infested nilgai. The possible utility of man-made barriers for R. microplus eradication in the lower part of the South Texas coastal plain wildlife corridor is discussed. Published by Oxford University Press on behalf of Entomological Society of America 2020.The association between aromatase inhibitors and cardiovascular outcomes is controversial. While some observational studies have assessed their cardiovascular safety as up-front treatments, their cardiotoxic effects as sequential treatments with tamoxifen remains unknown. Thus, we conducted a population-based cohort study using the United Kingdom Clinical Practice Research Datalink linked to the Hospital Episode Statistics and Office for National Statistics databases. A prevalent new-user design was used to propensity score match, in a 12 ratio, patients switching from tamoxifen to aromatase inhibitors to patients continuing tamoxifen between 1998 and 2016. Cox proportional hazards models were used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for the study outcomes (myocardial infarction, ischemic stroke, heart failure, and cardiovascular mortality). Overall, 1,962 patients switching to aromatase inhibitors were matched to 3,874 patients continuing tamoxifen. Compared with tamoxifen, aromatase inhibitors were associated with an increased risk of myocardial infarction (HR=2.08; 95% CI 1.02, 4.27). selleck chemicals llc The hazard ratio was elevated with ischemic stroke (HR=1.58; 95% CI 0.85, 2.93), heart failure (HR=1.69; 95% CI 0.79, 3.62), but not cardiovascular mortality (HR=0.87; 95% CI 0.49, 1.54), with CIs including the null. The elevated HRs observed for the cardiovascular outcomes should be corroborated in future large observational studies. © The Author(s) 2020. Published by Oxford University Press on behalf of the Johns Hopkins Bloomberg School of Public Health. All rights reserved. For permissions, please e-mail [email protected] squamous cell carcinoma (LSCC) is a highly disabling disease to the patient, affecting speech, swallowing and respiratory skills. Smoking and alcohol abuse are principal risk factors linked to this disease. Genetic factors can be involved in carcinogenesis by controlling the cell cycle, cell survival, angiogenesis, and invasiveness. Single nucleotide polymorphisms (SNPs) involving specific genes could modulate the risk of LSCC related to known carcinogens by modifying cellular responses, but not all genetic associations are known. In a case-control study, we assess the associations between cyclooxygenase-2 (COX2), epidermal growth factor (EGF), EGF receptor (EGFR), and tumor suppressor P53 SNPs on the risk of LSCC development in the Chilean population. A total of 85 LSCC patients and 95 healthy volunteers were recruited. SNPs genotype were analyzed from genomic DNA by Polymerase Chain Reaction (PCR)-Restriction Fragment Length Polymorphism (RFLP) and associations were estimated by odds ratios (ORs) using unconditional logistic regressions. A significant association between COX2 and TP53 SNP and LSCC risk was found, with an OR = 3.27 for COX2 c.-1329A>G (rs689466) SNP, and an OR = 1.94 for TP53 c.215C>G, Pro72Arg (rs1042522) SNP. These findings suggest that COX2 c.-1329A>G and TP53 c.215C>G (Pro72Arg) SNPs may be risk factors for LSCC. Through this research, we identify two low penetrance genetic variants that may be evaluated as novel biomarkers for this disease, in South American Mestizo populations. © 2020 The Author(s).
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