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Tytuł pozycji:

Long non-coding RNA DLEU2 drives EMT and glycolysis in endometrial cancer through HK2 by competitively binding with miR-455 and by modulating the EZH2/miR-181a pathway.

Tytuł:
Long non-coding RNA DLEU2 drives EMT and glycolysis in endometrial cancer through HK2 by competitively binding with miR-455 and by modulating the EZH2/miR-181a pathway.
Autorzy:
Dong P; Department of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, 0608638, Japan. .
Xiong Y; Department of Gynecology, State Key Laboratory of Oncology in South China, Sun Yat-sen University Cancer Center, Guangzhou, 510060, China.
Konno Y; Department of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, 0608638, Japan. .
Ihira K; Department of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, 0608638, Japan.
Kobayashi N; Department of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, 0608638, Japan.
Yue J; Department of Pathology and Laboratory Medicine, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.; Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Watari H; Department of Obstetrics and Gynecology, Hokkaido University School of Medicine, Hokkaido University, Sapporo, 0608638, Japan.
Źródło:
Journal of experimental & clinical cancer research : CR [J Exp Clin Cancer Res] 2021 Jun 26; Vol. 40 (1), pp. 216. Date of Electronic Publication: 2021 Jun 26.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: 2009- : London : BioMed Central
Original Publication: [Roma] : APSIT,
MeSH Terms:
Enhancer of Zeste Homolog 2 Protein/*genetics
Hexokinase/*genetics
MicroRNAs/*genetics
RNA, Long Noncoding/*genetics
Cell Line, Tumor ; Endometrial Neoplasms/genetics ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Glycolysis ; Humans ; Prognosis ; Signal Transduction ; Survival Analysis ; Up-Regulation
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Grant Information:
18K09278 Japan Society for the Promotion of Science; 19K09769 Japan Society for the Promotion of Science; 1R21CA216585-01A1 United States CA NCI NIH HHS
Contributed Indexing:
Keywords: Aerobic glycolysis; DLEU2; EMT; ERK1/2 signaling; Endometrial cancer; FAK; HK2; LncRNA; Long noncoding RNA; MicroRNA
Substance Nomenclature:
0 (DLEU2 lncRNA, human)
0 (MIRN455 microRNA, human)
0 (MIrn181 microRNA, human)
0 (MicroRNAs)
0 (RNA, Long Noncoding)
EC 2.1.1.43 (EZH2 protein, human)
EC 2.1.1.43 (Enhancer of Zeste Homolog 2 Protein)
EC 2.7.1.1 (HK2 protein, human)
EC 2.7.1.1 (Hexokinase)
Entry Date(s):
Date Created: 20210627 Date Completed: 20211206 Latest Revision: 20211214
Update Code:
20240105
PubMed Central ID:
PMC8235565
DOI:
10.1186/s13046-021-02018-1
PMID:
34174908
Czasopismo naukowe
Background: Epithelial-to-mesenchymal transition (EMT) and aerobic glycolysis are fundamental processes implicated in cancer metastasis. Although increasing evidence demonstrates an association between EMT induction and enhanced aerobic glycolysis in human cancer, the mechanisms linking these two conditions in endometrial cancer (EC) cells remain poorly defined.
Methods: We characterized the role and molecular mechanism of the glycolytic enzyme hexokinase 2 (HK2) in mediating EMT and glycolysis and investigated how long noncoding RNA DLEU2 contributes to the stimulation of EMT and glycolysis via upregulation of HK2 expression.
Results: HK2 was highly expressed in EC tissues, and its expression was associated with poor overall survival. Overexpression of HK2 effectively promoted EMT phenotypes and enhanced aerobic glycolysis in EC cells via activating FAK and its downstream ERK1/2 signaling. Moreover, microRNA-455 (miR-455) served as a tumor suppressor by directly interacting with HK2 mRNA and inhibiting its expression. Furthermore, DLEU2 displayed a significantly higher expression in EC tissues, and increased DLEU2 expression was correlated with worse overall survival. DLEU2 acted as an upstream activator for HK2-induced EMT and glycolysis in EC cells through two distinct mechanisms: (i) DLEU2 induced HK2 expression by competitively binding with miR-455, and (ii) DLEU2 also interacted with EZH2 to silence a direct inhibitor of HK2, miR-181a.
Conclusions: This study identified DLEU2 as an upstream activator of HK2-driven EMT and glycolysis in EC cells and provided significant mechanistic insights for the potential treatment of EC.
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