The natural genetic variation in pre-miR-146a affects the amount of mature miR-146a, contributes to the genetic predisposition to CaP.

MicroRNAs have been implicated in regulating diverse cellular pathways. Emerging evidence indicates that miR-143 plays causal roles in cancer tumorigenesis as a tumor suppress gene; however, its role in prostate cancer tumorigenesis remains largely unknown. The aims of this study were to verify the effect of miR-143 on proliferation and migration abilities of prostate cancer cells. The expression level of miR-143 and its target gene KRAS were measured by realtime PCR and western blotting, respectively. Effects of miR-143 in cell proliferation, migration and chemosensitivity were evaluated by MTT assay, FACS cell cycle analysis, colony formation assay, and transwell migratory assay. Our results revealed an inverse correlation of expression between miR-143 and KRAS protein in prostate cancer samples (Pearson's correlation scatter plots: R = -0.707, P < 0.05). Moreover, over-expression of miR-143 in prostate cancer cells suppressed their proliferation and migration and increased their sensitivity to docetaxel by targeting EGFR/RAS/MAPK pathway. These findings suggest that miR-143 plays an important role in prostate cancer proliferation, migration and chemosensitivity by suppressing KRAS and subsequent inactivation of MAPK pathway, which provides a potential development of a new approach for the treatment of prostate cancer.

Background: Psoriasis is a common, chronic, inflammatory, debilitating, systemic disease with a great impact on healthcare systems worldwide. As targeted therapies have transformed the therapeutic landscape, updated estimates of the Global Burden of Disease (GBD) imposed by psoriasis are necessary in order to evaluate the effects of past health care policies and to orient and inform new national and international healthcare strategies.Methods: Data were extracted from the GBD 2019 study, which collates a systematic review of relevant scientific literature, national surveys, claims data, and primary care sources on the prevalence of psoriasis. Prevalence data were combined with disability weight (DW) to yield years lived with disability (YLDs). Measures of burden at global, regional, and national levels were generated for incidence, prevalence, and YLDs, due to psoriatic disease. All measures were reported as absolute numbers, percentages, and crude and age-adjusted rates per 100,000 persons. In addition, psoriasis burden was assessed by socio-demographic index (SDI).Findings: According to the GBD 2019 methodology, there were 4,622,594 (95% uncertainty interval or UI 4,458,904–4,780,771) incident cases of psoriasis worldwide in 2019. The age-standardized incidence rate in 2019 was 57.8 (95% UI 55.8–59.7) per 100,000 people. With respect to 1990, this corresponded to a decrease of 20.0% (95% UI −20.2 to −19.8). By sex, the age-standardized incidence rate was similar between men [57.8 (95% UI 55.8–59.8) per 100,000 people] and women [(57.8 (95% UI 55.8–59.7) per 100,000 people]. With respect to 1990, this corresponded to a decrease by 19.5% (95% UI −19.8 to −19.2) and by 20.4% (95% UI −20.7 to −20.2) for men and women, respectively. The age-standardized incidence rate per 100,000 persons was found to vary widely across geographic locations. Regionally, high-income countries and territories had the highest age-standardized incidence rate of psoriasis [112.6 (95% UI 108.9–116.1)], followed by high-middle SDI countries [69.4 (95% UI 67.1–71.9)], while low SDI countries reported the lowest rate [38.1 (95% UI 36.8–39.5)]. Similar trends were detected for prevalence and YLDs.Conclusion: In general, psoriasis burden is greatest in the age group of 60–69 years, with a relatively similar burden among men and women. The burden is disproportionately greater in high-income and high SDI index countries of North America and Europe. With advances in psoriasis therapeutics, objective evaluation of psoriasis disease burden is critical to track the progress at the population level.

Abstract.It has been shown that regulation of EGFR expression in prostate cancer cells is mostly at the transcriptional level. microRNA-133 (miR-133) has long been recognized as a muscle-specific miRNA which may regulate myoblast differentiation and participate in many myogenic diseases. Recently, it has been reported that miR-133 is also involved in other tumors, such as bladder cancer, esophageal cancer and may regulate cell motility in these cancer cells. In the present study, we examined the expression and effects of miR-133 in two hormone-insensitive prostate cancer cell lines. The expression of miR-133a and miR-133b were analyzed by quantitative RT-PCR. After transfection of miR-133a and miR-133b, cell viability assay, luciferase assay, western blot analysis, cell migration and invasion assay were conducted in DU145 and PC3 cells. In this study, we showed that miR-133a and miR-133b are expressed at the detection limit in two hormoneinsensitive prostate cancer cell lines, PC3 and DU145. Ectopic expression of miR-133 inhibited cell proliferation, migration and invasion in these cells. We also provide the first evidence that miR-133 may target EGFR. Our study provided the first glimpse of the functional role of miR-133 in two hormoneindependent prostate cancer cell lines. These results may add to our knowledge on the molecular basis of prostate cancer progression.

Room temperature continuous-wave operation of InAsSb quantum-dot distributed feedback lasers Appl. Phys. Lett. 87, 203102 (2005); 10.1063/1.2130527 Room-temperature continuous-wave operation of InAsSb quantum-dot lasers near 2 μm based on (001) InP substrate Appl.

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Dysregulation of chromobox proteins contributes to the progression of human diseases. CBX1 has been implicated in epigenetic control of chromatin structure and gene expression, but its role in human cancers remains largely unknown. Here we show that CBX1 exhibits oncogenic activities in hepatocellular carcinoma (HCC) and indicates poor outcomes. The expression of CBX1 was noticeably increased, at both mRNA and protein levels, in HCC tissues and cell lines, compared with the nontumorous ones. High CBX1 expression was significantly associated with larger tumor size, poor tumor differentiation and tumor vascular invasion. Patients with elevated expression of CBX1 were frequently accompanied with unfavorable overall and disease-free survivals in two independent cohorts consisting of 648 HCC cases. The prognostic value of CBX1 was further confirmed by stratified survival analyses. Multivariate cox regression model suggested CBX1 as an independent factor for overall survival (hazard ratio = 1.735, 95% confident interval: 1.342–2.244, P < .001). In vitro data demonstrated that CBX1 overexpression promoted cell proliferation and migration, whereas the knockdown of CBX1 resulted in the opposite phenotypes. Mechanistically, CBX1 interacted with transcription factor HMGA2 to activate the Wnt/β-Catenin signaling pathway. Suppression of β-Catenin by siRNA or specific inhibitor XAV-939 markedly attenuated CBX1-mediated cell growth. Collectively, our findings indicate that CBX1 functions as an oncogene and may serve as a potential prognostic biomarker in HCC.

This study provided the first glimpse of the functional role of miR-133 in bladder cancer T24 and EJ cells. The results may increase our knowledge on the molecular basis of progression and provide potential therapy for bladder cancer.