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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
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| Title: | 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 |
| Authors: | Dong, Peixin Browse this author →KAKEN DB | | Xiong, Ying Browse this author | | Konno, Yosuke Browse this author | | Ihira, Kei Browse this author | | Kobayashi, Noriko Browse this author | | Yue, Junming Browse this author | | Watari, Hidemichi Browse this author |
| Keywords: | HK2 | | FAK | | ERK1/2 signaling | | DLEU2 | | Long noncoding RNA | | LncRNA | | MicroRNA | | EMT | | Aerobic glycolysis | | Endometrial cancer |
| Issue Date: | 26-Jun-2021 |
| Journal Title: | Journal of Experimental & Clinical Cancer Research |
| Volume: | 40 |
| Start Page: | 216 |
| Publisher DOI: | 10.1186/s13046-021-02018-1 |
| Abstract: | 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. |
| Rights: | http://creativecommons.org/licenses/by/4.0/ |
| Type: | article |
| URI: | http://hdl.handle.net/2115/82149 |
| Appears in Collections: | 医学院・医学研究院 (Graduate School of Medicine / Faculty of Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 董 培新
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