Matches in SemOpenAlex for { <https://semopenalex.org/work/W2617141566> ?p ?o ?g. }
- W2617141566 endingPage "65217" @default.
- W2617141566 startingPage "65211" @default.
- W2617141566 abstract "// Hongxia Yao 1, * , Pei Sun 2, * , Mengling Duan 1, * , Lie Lin 1 , Yanping Pan 1 , Congming Wu 1 , Xiangjun Fu 1 , Hua Wang 1 , Li Guo 1 , Tianbo Jin 3 and Yipeng Ding 4 1 Department of Hematology, Hainan General Hospital, Haikou, Hainan 570311, P.R. China 2 Department of Hematology, Hunan Yiyang Central Hospital, Yiyang, Hunan 413000, P.R. China 3 Key Laboratory of Resource Biology and Biotechnology in Western China (Northwest University), Ministry of Education, Xi’an, Shaanxi 710069, P.R. China 4 Department of Emergency, Hainan General Hospital, Haikou, Hainan 570311, P.R. China * These authors have contributed equally to this work Correspondence to: Hongxia Yao, email: yaohongxiahk@163.com Yipeng Ding, email: ypding@263.net Keywords: acute myeloid leukemia(AML), MEG3, long non-coding RNA, TET2, miR-22-3p/5p Received: March 22, 2017 Accepted: April 19, 2017 Published: May 22, 2017 ABSTRACT Aim: Acute myeloid leukemia (AML) is the most common blood tumor with poor prognosis. At present, the research found that the pathogenesis of AML is related to many factors, such as recurrent somatic mutations and gene expression and epigenetic changes, however, the molecular mechanism of AML is still unclear. Long non-coding RNA MEG3 is a newly found tumor suppressor and plays a very important role in the regulation of a variety of tumor formation and progression. Studies found that the MEG3 expression was significantly decreased in AML. However, to date, it is not clear the cause of its abnormal expression. Therefore, the molecular mechanism of AML is urgently needed to study the molecular mechanism of AML. Methods: The different expression level of MEG3, TET2, miR-22-3p, miR-22-5p in AML was detected by real-time quantification PCR. MEG3, TET2, miR-22-3p, miR-22-3p expression cell pools in K562 cells was used to interfering and TET2, MEG3 TET2, relations with miR-22-3p, miR-22-5p. The effect of AML cell on proliferation was evaluated by TET2 lower expression. Results: 1. The lower expression of MEG3 and TET2 in AML cell lines was detected by RT-qPCR. 2. The stable MEG3, TET2 overexpression cell pools in K562 cells was successful established. 3. After transfection, MTT assay revealed that cell growth was significantly increased in AML cell lines transfected with TET2 compared with controls. Conclusions: Our findings suggested that MEG3 is significantly down regulated in AML cell lines." @default.
- W2617141566 created "2017-06-05" @default.
- W2617141566 creator A5001660941 @default.
- W2617141566 creator A5006872013 @default.
- W2617141566 creator A5014336437 @default.
- W2617141566 creator A5026487938 @default.
- W2617141566 creator A5037309725 @default.
- W2617141566 creator A5047633478 @default.
- W2617141566 creator A5053725057 @default.
- W2617141566 creator A5058598970 @default.
- W2617141566 creator A5064905193 @default.
- W2617141566 creator A5083531621 @default.
- W2617141566 creator A5089823522 @default.
- W2617141566 date "2017-05-22" @default.
- W2617141566 modified "2023-10-17" @default.
- W2617141566 title "microRNA-22 can regulate expression of the long non-coding RNA MEG3 in acute myeloid leukemia" @default.
- W2617141566 cites W1849240407 @default.
- W2617141566 cites W1964866117 @default.
- W2617141566 cites W1970145665 @default.
- W2617141566 cites W1977846137 @default.
- W2617141566 cites W1979906856 @default.
- W2617141566 cites W1981463058 @default.
- W2617141566 cites W1989126702 @default.
- W2617141566 cites W1993701888 @default.
- W2617141566 cites W1997453048 @default.
- W2617141566 cites W2003544524 @default.
- W2617141566 cites W2010914889 @default.
- W2617141566 cites W2023346582 @default.
- W2617141566 cites W2049482339 @default.
- W2617141566 cites W2061427860 @default.
- W2617141566 cites W2066815559 @default.
- W2617141566 cites W2075543245 @default.
- W2617141566 cites W2075952448 @default.
- W2617141566 cites W2083033504 @default.
- W2617141566 cites W2095293920 @default.
- W2617141566 cites W2095340797 @default.
- W2617141566 cites W2097743943 @default.
- W2617141566 cites W2105349784 @default.
- W2617141566 cites W2105926260 @default.
- W2617141566 cites W2108664872 @default.
- W2617141566 cites W2108718836 @default.
- W2617141566 cites W2109150359 @default.
- W2617141566 cites W2112129429 @default.
- W2617141566 cites W2119576141 @default.
- W2617141566 cites W2134944515 @default.
- W2617141566 cites W2164252048 @default.
- W2617141566 cites W2170552969 @default.
- W2617141566 cites W2221725900 @default.
- W2617141566 cites W4238020764 @default.
- W2617141566 doi "https://doi.org/10.18632/oncotarget.18059" @default.
- W2617141566 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/5630324" @default.
- W2617141566 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/29029424" @default.
- W2617141566 hasPublicationYear "2017" @default.
- W2617141566 type Work @default.
- W2617141566 sameAs 2617141566 @default.
- W2617141566 citedByCount "22" @default.
- W2617141566 countsByYear W26171415662017 @default.
- W2617141566 countsByYear W26171415662018 @default.
- W2617141566 countsByYear W26171415662019 @default.
- W2617141566 countsByYear W26171415662020 @default.
- W2617141566 countsByYear W26171415662021 @default.
- W2617141566 countsByYear W26171415662022 @default.
- W2617141566 countsByYear W26171415662023 @default.
- W2617141566 crossrefType "journal-article" @default.
- W2617141566 hasAuthorship W2617141566A5001660941 @default.
- W2617141566 hasAuthorship W2617141566A5006872013 @default.
- W2617141566 hasAuthorship W2617141566A5014336437 @default.
- W2617141566 hasAuthorship W2617141566A5026487938 @default.
- W2617141566 hasAuthorship W2617141566A5037309725 @default.
- W2617141566 hasAuthorship W2617141566A5047633478 @default.
- W2617141566 hasAuthorship W2617141566A5053725057 @default.
- W2617141566 hasAuthorship W2617141566A5058598970 @default.
- W2617141566 hasAuthorship W2617141566A5064905193 @default.
- W2617141566 hasAuthorship W2617141566A5083531621 @default.
- W2617141566 hasAuthorship W2617141566A5089823522 @default.
- W2617141566 hasBestOaLocation W26171415661 @default.
- W2617141566 hasConcept C104317684 @default.
- W2617141566 hasConcept C126322002 @default.
- W2617141566 hasConcept C143998085 @default.
- W2617141566 hasConcept C145059251 @default.
- W2617141566 hasConcept C194409129 @default.
- W2617141566 hasConcept C2778461978 @default.
- W2617141566 hasConcept C2778729363 @default.
- W2617141566 hasConcept C2781369401 @default.
- W2617141566 hasConcept C41091548 @default.
- W2617141566 hasConcept C502942594 @default.
- W2617141566 hasConcept C54355233 @default.
- W2617141566 hasConcept C62203573 @default.
- W2617141566 hasConcept C67705224 @default.
- W2617141566 hasConcept C71924100 @default.
- W2617141566 hasConcept C86803240 @default.
- W2617141566 hasConceptScore W2617141566C104317684 @default.
- W2617141566 hasConceptScore W2617141566C126322002 @default.
- W2617141566 hasConceptScore W2617141566C143998085 @default.
- W2617141566 hasConceptScore W2617141566C145059251 @default.
- W2617141566 hasConceptScore W2617141566C194409129 @default.
- W2617141566 hasConceptScore W2617141566C2778461978 @default.
- W2617141566 hasConceptScore W2617141566C2778729363 @default.