FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2768493050> ?p ?o ?g. }

• W2768493050 endingPage "111245" @default.
• W2768493050 startingPage "111225" @default.
• W2768493050 abstract "// Giovanni Luca Gravina 1, 2 , Andrea Mancini 1 , Alessandro Colapietro 1 , Francesco Marampon 1 , Roberta Sferra 3 , Simona Pompili 3 , Leda Assunta Biordi 4 , Roberto Iorio 5 , Vincenzo Flati 4 , Christian Argueta 6 , Yosef Landesman 6 , Michael Kauffman 6 , Sharon Shacham 6 and Claudio Festuccia 1 1 Department of Biotechnological and Applied Clinical Sciences, Laboratory of Radiobiology, University of L’Aquila, L’Aquila, Italy 2 Department of Biotechnological and Applied Clinical Sciences, Division of Radiotherapy, University of L’Aquila, L’Aquila, Italy 3 Department of Biotechnological and Applied Clinical Sciences, Division of Human Anatomy, University of L’Aquila, L’Aquila, Italy 4 Department of Biotechnological and Applied Clinical Sciences, Division of Molecular Pathology, University of L’Aquila, L’Aquila, Italy 5 Department of Biotechnological and Applied Clinical Sciences, Division of Applied Biology, University of L’Aquila, L’Aquila, Italy 6 Karyopharm Therapeutics, Newton, MA, USA Correspondence to: Claudio Festuccia, email: claudio.festuccia@univaq.it Keywords: castration resistant prostate cancer (CrPCa); chromosome region maintenance (CRM-1); exportin-1 (XPO-1); selective inhibitors of nuclear export (SINE); docetaxel (DTX) Received: June 29, 2017     Accepted: November 13, 2017     Published: November 30, 2017 ABSTRACT Background and aims: Docetaxel (DTX) modestly increases patient survival of metastatic castration-resistant prostate cancer (mCRPC) due to insurgence of pharmacological resistance. Deregulation of Chromosome Region Maintenance (CRM-1)/ exportin-1 (XPO-1)-mediated nuclear export may play a crucial role in this phenomenon. Material and methods: Here, we evaluated the effects of two Selective Inhibitor of Nuclear Export (SINE) compounds, selinexor (KPT-330) and KPT-251, in association with DTX by using 22rv1, PC3 and DU145 cell lines with their. DTX resistant derivatives. Results and conclusions: We show that DTX resistance may involve overexpression of β-III tubulin (TUBB3) and P-glycoprotein as well as increased cytoplasmic accumulation of Foxo3a. Increased levels of XPO-1 were also observed in DTX resistant cells suggesting that SINE compounds may modulate DTX effectiveness in sensitive cells as well as restore the sensitivity to DTX in resistant ones. Pretreatment with SINE compounds, indeed, sensitized to DTX through increased tumor shrinkage and apoptosis by preventing DTX-induced cell cycle arrest. Basally SINE compounds induce FOXO3a activation and nuclear accumulation increasing the expression of FOXO-responsive genes including p21, p27 and Bim causing cell cycle arrest. SINE compounds-catenin and survivin supporting apoptosis. βdown-regulated Cyclin D1, c-myc, Nuclear sequestration of p-Foxo3a was able to reduce ABCB1 and TUBB3 H2AX levels, prolonged γ expression. Selinexor treatment increased DTX-mediated double strand breaks (DSB), and reduced the levels of DNA repairing proteins including DNA PKc and Topo2A. Our results provide supportive evidence for the therapeutic use of SINE compounds in combination with DTX suggesting their clinical use in mCRPC patients." @default.
• W2768493050 created "2017-12-04" @default.
• W2768493050 creator A5002876711 @default.
• W2768493050 creator A5008951735 @default.
• W2768493050 creator A5011273738 @default.
• W2768493050 creator A5015865144 @default.
• W2768493050 creator A5026640374 @default.
• W2768493050 creator A5030295135 @default.
• W2768493050 creator A5039243219 @default.
• W2768493050 creator A5047952766 @default.
• W2768493050 creator A5051278445 @default.
• W2768493050 creator A5051352882 @default.
• W2768493050 creator A5057755017 @default.
• W2768493050 creator A5071420169 @default.
• W2768493050 creator A5076187874 @default.
• W2768493050 creator A5080888531 @default.
• W2768493050 date "2017-11-30" @default.
• W2768493050 modified "2023-10-18" @default.
• W2768493050 title "Pharmacological treatment with inhibitors of nuclear export enhances the antitumor activity of docetaxel in human prostate cancer" @default.
• W2768493050 cites W1492131844 @default.
• W2768493050 cites W171333759 @default.
• W2768493050 cites W1886771640 @default.
• W2768493050 cites W1964824076 @default.
• W2768493050 cites W1979070712 @default.
• W2768493050 cites W1982727560 @default.
• W2768493050 cites W1987295322 @default.
• W2768493050 cites W1988975697 @default.
• W2768493050 cites W2011193086 @default.
• W2768493050 cites W2013800509 @default.
• W2768493050 cites W2015050458 @default.
• W2768493050 cites W2020579083 @default.
• W2768493050 cites W2023097049 @default.
• W2768493050 cites W2028972576 @default.
• W2768493050 cites W2041620567 @default.
• W2768493050 cites W2047222465 @default.
• W2768493050 cites W2053897072 @default.
• W2768493050 cites W2055763886 @default.
• W2768493050 cites W2057433540 @default.
• W2768493050 cites W2058033508 @default.
• W2768493050 cites W2059944478 @default.
• W2768493050 cites W2064497478 @default.
• W2768493050 cites W2064899027 @default.
• W2768493050 cites W2079113237 @default.
• W2768493050 cites W2082739624 @default.
• W2768493050 cites W2085325354 @default.
• W2768493050 cites W2086354663 @default.
• W2768493050 cites W2090583090 @default.
• W2768493050 cites W2095967369 @default.
• W2768493050 cites W2096439168 @default.
• W2768493050 cites W2096849855 @default.
• W2768493050 cites W2099129345 @default.
• W2768493050 cites W2101096891 @default.
• W2768493050 cites W2106572206 @default.
• W2768493050 cites W2110942624 @default.
• W2768493050 cites W2116010205 @default.
• W2768493050 cites W2117051942 @default.
• W2768493050 cites W2122952432 @default.
• W2768493050 cites W2123726946 @default.
• W2768493050 cites W2126583835 @default.
• W2768493050 cites W2128518191 @default.
• W2768493050 cites W2130287531 @default.
• W2768493050 cites W2137293812 @default.
• W2768493050 cites W2140382280 @default.
• W2768493050 cites W2154558136 @default.
• W2768493050 cites W2156025284 @default.
• W2768493050 cites W2158204878 @default.
• W2768493050 cites W2169669596 @default.
• W2768493050 cites W2169727232 @default.
• W2768493050 cites W2169896143 @default.
• W2768493050 cites W2171237698 @default.
• W2768493050 cites W2179708332 @default.
• W2768493050 cites W2187721367 @default.
• W2768493050 cites W2236127431 @default.
• W2768493050 cites W2285097862 @default.
• W2768493050 cites W2298048863 @default.
• W2768493050 cites W2301608130 @default.
• W2768493050 cites W2313842338 @default.
• W2768493050 cites W2342798889 @default.
• W2768493050 cites W2400503972 @default.
• W2768493050 cites W2400794200 @default.
• W2768493050 cites W2510940971 @default.
• W2768493050 cites W2526506448 @default.
• W2768493050 cites W2528134649 @default.
• W2768493050 cites W2528748907 @default.
• W2768493050 cites W2531688834 @default.
• W2768493050 cites W2567743670 @default.
• W2768493050 cites W2571996409 @default.
• W2768493050 cites W2598884790 @default.
• W2768493050 cites W2618815950 @default.
• W2768493050 cites W2987371202 @default.
• W2768493050 cites W4232324806 @default.
• W2768493050 doi "https://doi.org/10.18632/oncotarget.22760" @default.
• W2768493050 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6824873" @default.
• W2768493050 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31695847" @default.
• W2768493050 hasPublicationYear "2017" @default.
• W2768493050 type Work @default.
• W2768493050 sameAs 2768493050 @default.
• W2768493050 citedByCount "16" @default.

• next