FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2340484061> ?p ?o ?g. }

• W2340484061 endingPage "18650" @default.
• W2340484061 startingPage "18638" @default.
• W2340484061 abstract "// Houcai Wang 1, * , Bingqian Xie 1, * , Yuanyuan Kong 1, * , Yi Tao 1 , Guang Yang 1 , Minjie Gao 1 , Hongwei Xu 2 , Fenghuang Zhan 2 , Jumei Shi 1 , Yiwen Zhang 1 , Xiaosong Wu 1 1 Department of Hematology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai, China 2 Department of Internal Medicine, University of Iowa, Carver College of Medicine, Iowa, USA * These authors contributed equally to this work Correspondence to: Jumei Shi, e-mail: shijumei@tongji.edu.cn Yiwen Zhang, e-mail: ahzhyw@126.com Xiaosong Wu, e-mail: wux163@163.com Keywords: STAT3, RPS27a, imatinib, apoptosis, CML Received: November 11, 2015      Accepted: February 13, 2016      Published: March 03, 2016 ABSTRACT STAT3 plays a pivotal role in the hematopoietic system, which constitutively activated by BCR–ABL via JAK and Erk/MAP-kinase pathways. Phospho-STAT3 was overexpressed in imatinib-resistant CML patients as relative to imatinib responsive ones. By activation of the STAT3 pathway, BCR–ABL can promote cell cycling, and inhibit differentiation and apoptosis. Ribosomal protein S27a (RPS27a) performs extra-ribosomal functions besides imparting a role in ribosome biogenesis and post-translational modifications of proteins. RPS27a can promote proliferation, regulate cell cycle progression and inhibit apoptosis of leukemia cells. However, the relationship between STAT3 and RPS27a has not been reported. In this study, we detected a significantly increased expression of STAT3 and RPS27a in bone marrow samples from CML-AP/BP patients compared with those from CML-CP. In addition, we also demonstrated that it was a positive correlation between the level of STAT3 and that of RPS27a. Imatinib-resistant K562/G01 cells expressed significantly higher levels of STAT3 and RPS27a compared with those of K562 cells. RPS27a could be transactivated by p-STAT3 through the specific p-STAT3-binding site located nt −633 to −625 and −486 to −478 of the RPS27a gene promoter in a dose-dependent manner. The transactivated RPS27a could decrease the percentage of apoptotic CML cells induced by imatinib. And the effect of STAT3 overexpression could be counteracted by the p-STAT3 inhibitor WP1066 or RPS27a knockdown. These results suggest that drugs targeting STAT3/p-STAT3/RPS27a combining with TKI might represent a novel therapy strategy in patients with TKI-resistant CML." @default.
• W2340484061 created "2016-06-24" @default.
• W2340484061 creator A5002787785 @default.
• W2340484061 creator A5012108815 @default.
• W2340484061 creator A5032155470 @default.
• W2340484061 creator A5038653609 @default.
• W2340484061 creator A5045909068 @default.
• W2340484061 creator A5056904374 @default.
• W2340484061 creator A5070245791 @default.
• W2340484061 creator A5073693517 @default.
• W2340484061 creator A5079392856 @default.
• W2340484061 creator A5080177478 @default.
• W2340484061 creator A5089586496 @default.
• W2340484061 date "2016-03-03" @default.
• W2340484061 modified "2023-10-18" @default.
• W2340484061 title "Overexpression of RPS27a contributes to enhanced chemoresistance of CML cells to imatinib by the transactivated STAT3" @default.
• W2340484061 cites W1484459469 @default.
• W2340484061 cites W1598129325 @default.
• W2340484061 cites W1851477645 @default.
• W2340484061 cites W1966400945 @default.
• W2340484061 cites W1968975746 @default.
• W2340484061 cites W1975090733 @default.
• W2340484061 cites W1978514731 @default.
• W2340484061 cites W1987060590 @default.
• W2340484061 cites W1997049152 @default.
• W2340484061 cites W1997254819 @default.
• W2340484061 cites W1999614615 @default.
• W2340484061 cites W2002658208 @default.
• W2340484061 cites W2003792568 @default.
• W2340484061 cites W2016656445 @default.
• W2340484061 cites W2029478248 @default.
• W2340484061 cites W2031212307 @default.
• W2340484061 cites W2033398667 @default.
• W2340484061 cites W2040802938 @default.
• W2340484061 cites W2043122200 @default.
• W2340484061 cites W2050237470 @default.
• W2340484061 cites W2051674520 @default.
• W2340484061 cites W2054086725 @default.
• W2340484061 cites W2058576674 @default.
• W2340484061 cites W2069642052 @default.
• W2340484061 cites W2082469361 @default.
• W2340484061 cites W2082865738 @default.
• W2340484061 cites W2088412411 @default.
• W2340484061 cites W2097255369 @default.
• W2340484061 cites W2101390452 @default.
• W2340484061 cites W2103553801 @default.
• W2340484061 cites W2108689358 @default.
• W2340484061 cites W2125942629 @default.
• W2340484061 cites W2134259065 @default.
• W2340484061 cites W2141094258 @default.
• W2340484061 cites W2142969636 @default.
• W2340484061 cites W2329648702 @default.
• W2340484061 cites W2404194811 @default.
• W2340484061 doi "https://doi.org/10.18632/oncotarget.7888" @default.
• W2340484061 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4951316" @default.
• W2340484061 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26942564" @default.
• W2340484061 hasPublicationYear "2016" @default.
• W2340484061 type Work @default.
• W2340484061 sameAs 2340484061 @default.
• W2340484061 citedByCount "19" @default.
• W2340484061 countsByYear W23404840612016 @default.
• W2340484061 countsByYear W23404840612017 @default.
• W2340484061 countsByYear W23404840612019 @default.
• W2340484061 countsByYear W23404840612020 @default.
• W2340484061 countsByYear W23404840612021 @default.
• W2340484061 countsByYear W23404840612022 @default.
• W2340484061 countsByYear W23404840612023 @default.
• W2340484061 crossrefType "journal-article" @default.
• W2340484061 hasAuthorship W2340484061A5002787785 @default.
• W2340484061 hasAuthorship W2340484061A5012108815 @default.
• W2340484061 hasAuthorship W2340484061A5032155470 @default.
• W2340484061 hasAuthorship W2340484061A5038653609 @default.
• W2340484061 hasAuthorship W2340484061A5045909068 @default.
• W2340484061 hasAuthorship W2340484061A5056904374 @default.
• W2340484061 hasAuthorship W2340484061A5070245791 @default.
• W2340484061 hasAuthorship W2340484061A5073693517 @default.
• W2340484061 hasAuthorship W2340484061A5079392856 @default.
• W2340484061 hasAuthorship W2340484061A5080177478 @default.
• W2340484061 hasAuthorship W2340484061A5089586496 @default.
• W2340484061 hasBestOaLocation W23404840611 @default.
• W2340484061 hasConcept C121608353 @default.
• W2340484061 hasConcept C126322002 @default.
• W2340484061 hasConcept C190283241 @default.
• W2340484061 hasConcept C2777583451 @default.
• W2340484061 hasConcept C2778729363 @default.
• W2340484061 hasConcept C2778923194 @default.
• W2340484061 hasConcept C29537977 @default.
• W2340484061 hasConcept C502942594 @default.
• W2340484061 hasConcept C54355233 @default.
• W2340484061 hasConcept C57074206 @default.
• W2340484061 hasConcept C62478195 @default.
• W2340484061 hasConcept C71924100 @default.
• W2340484061 hasConcept C75217442 @default.
• W2340484061 hasConcept C86803240 @default.
• W2340484061 hasConcept C95444343 @default.
• W2340484061 hasConceptScore W2340484061C121608353 @default.
• W2340484061 hasConceptScore W2340484061C126322002 @default.
• W2340484061 hasConceptScore W2340484061C190283241 @default.

• next