9 research outputs found
Possibilities and limitations of capillary gas chromatography and mass spectrometry in the analysis of polychlorinated biphenyls
The possibilities and limitations of analyses of polychlorinated biphenyls (PCBs) by capillary gas chromatography and capillary gas chromatography-mass spectrometry have been investigated. Metal capillary columns (WCOT) coated with Apiezon L and OV-101 were not suitable for PCB analyses. Good results were obtained in the separation of model mixtures of PCBs and of Aroclor 1242 on a glass capillary column coated with OV-101. Sources of error are indicated that may be encountered in the characterization of PCB components in Aroclor 1242 by standard additions, Kováts' retention indices and mass spectrometry. The direct coupling of a capillary column (WCOT) to a mass spectrometer produced spectra of the main PCB components, many of which could be used in the identification of isomeric PCBs
One-Year Follow-Up of Cystic Fibrosis Patients Who Cannot Reach the Modulator Therapies Although Having Indications: What are Their Losses?
Analysis of the relationship between the KRAS G12V oncogene and the Hippo effector YAP1 in embryonal rhabdomyosarcoma
Alginate oligosaccharide attenuates α2,6-sialylation modification to inhibit prostate cancer cell growth via the Hippo/YAP pathway
YAP1 and AR interactions contribute to the switch from androgen-dependent to castration-resistant growth in prostate cancer
The transcriptional co-activator Yes-associated protein 1 (YAP1), a key nuclear effector of the Hippo pathway, is a potent oncogene, and yet, the interaction between YAP1 and androgen receptor (AR) remains unexplored. Here we identify YAP1 as a physiological binding partner and positive regulator of AR in prostate cancer. YAP1 and AR co-localize and interact with each other predominantly within cell nuclei by an androgen-dependent mechanism in a hormone naive and an androgen-independent mechanism in castration-resistant prostate cancer cells. The growth suppressor MST1 kinase modulates androgen-dependent and -independent nuclear YAP1–AR interactions through directly regulating YAP1 nuclear accumulation. Disruption of YAP1 signalling by genetic (RNAi) and pharmacological (Verteporfin) approaches suppresses AR-dependent gene expression and prostate cancer cell growth. These findings indicate that the YAP1–AR axis may have a critical role in prostate cancer progression and serves as a viable drug target