E2F7−EZH2 axis regulates PTEN/AKT/mTOR signalling and glioblastoma progression

Yang, Rui; Wang, Mei; Zhang, Guanghui; Bao, Yonghua; Wu, Yanan; Li, Xiuxiu; Yang, Wancai; Cui, Hongjuan

doi:10.1038/s41416-020-01032-y

Cited by 61 publications

(46 citation statements)

References 49 publications

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“…All of the cell lines were authenticated and confirmed to be mycoplasma-free before use. All cells were cultured as previously described 17 .…”

Section: Methodsmentioning

confidence: 99%

“…MTT assay was employed to determining the ability of cell proliferation as described previously 17 .…”

Section: Methodsmentioning

confidence: 99%

“…PDPK1 promoter fragment and mutations of the consensus POU2F2-binding site were synthetic and constructed to pGL3-Basic. The plasmids transfection and lentiviruses infection were carried out as previously described 17 .…”

Section: Methodsmentioning

confidence: 99%

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POU2F2 regulates glycolytic reprogramming and glioblastoma progression via PDPK1-dependent activation of PI3K/AKT/mTOR pathway

et al. 2021

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The POU Class Homeobox 2 (POU2F2) is a member of POU transcription factors family, which involves in cell immune response by regulating B cell proliferation and differentiation genes. Recent studies have shown that POU2F2 acts as tumor-promoting roles in some cancers, but the underlying mechanism remains little known. Here, we identified that the highly expressed POU2F2 significantly correlated with poor prognosis of glioblastoma (GBM) patients. POU2F2 promoted cell proliferation and regulated glycolytic reprogramming. Mechanistically, the AKT/mTOR signaling pathway played important roles in the regulation of POU2F2-mediated aerobic glycolysis and cell growth. Furthermore, we demonstrated that POU2F2 activated the transcription of PDPK1 by directly binding to its promoter. Reconstituted the expression of PDPK1 in POU2F2-knockdown GBM cells reactivated AKT/mTOR pathway and recovered cell glycolysis and proliferation, whereas this effect was abolished by the PDPK1/AKT interaction inhibitor. In addition, we showed that POU2F2-PDPK1 axis promoted tumorigenesis by regulating glycolysis in vivo. In conclusion, our findings indicate that POU2F2 leads a metabolic shift towards aerobic glycolysis and promotes GBM progression in PDPK1-dependent activation of PI3K/AKT/mTOR pathway.

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“…All of the cell lines were authenticated and confirmed to be mycoplasma-free before use. All cells were cultured as previously described 17 .…”

Section: Methodsmentioning

confidence: 99%

“…MTT assay was employed to determining the ability of cell proliferation as described previously 17 .…”

Section: Methodsmentioning

confidence: 99%

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POU2F2 regulates glycolytic reprogramming and glioblastoma progression via PDPK1-dependent activation of PI3K/AKT/mTOR pathway

et al. 2021

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“…Immunohistochemical staining was carried as previous described ( 31 ). The antibodies HELLS (1:500; Santa Cruz, sc-46665) and GLUT1 (1:250; Abcam, ab115730) were used in this study.…”

Section: Methodsmentioning

confidence: 99%

MiR-365a-3p-Mediated Regulation of HELLS/GLUT1 Axis Suppresses Aerobic Glycolysis and Gastric Cancer Growth

et al. 2021

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Gastric cancer (GC) is a common and invasive malignancy, which lacks effective treatment and is the third main reason of cancer death. Metabolic reprogramming is one of the main reasons that GC is difficult to treat in various environments. Particularly, abnormal glycolytic activity is the most common way of metabolism reprogramming in cancer cells. Numerous studies have shown that microRNAs play important roles in reprogramming glucose metabolism. Here, we found a microRNA-miR-365a-3p, was significantly downregulated in GC according to bioinformatics analysis. Low expression of miR-365a-3p correlated with poor prognosis of GC patients. Overexpression of miR-365a-3p in GC cells significantly inhibited cell proliferation by inducing cell cycle arrest at G1 phase. Notably, miR-365a-3p induced downregulation of HELLS through binding to its 3′ untranslated region (UTR). Additionally, we found that miR-365a-3p suppressed aerobic glycolysis by inhibiting HELLS/GLUT1 axis. Lastly, we shown that overexpression of miR-365a-3p significantly inhibited tumor growth in nude mice. Conversely, Reconstituted the expression of HELLS rescued the suppressive effects of miR-365a-3p. Our data collectively indicated that miR-365a-3p functioned as a tumor suppressor in GC through downregulating HELLS. Therefore, targeting of the novel miR-365a-3p/HELLS axis could be a potentially effective therapeutic approach for GC.

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“…Recent studies have demonstrated that enhancer of zeste homolog 2 (EZH2) can promote cell cycle progression by affecting the PI3K/AKT pathway or the expression levels of cyclins (63)(64)(65). EZH2 can also be post-translationally modified by phosphorylation of AKT (66).…”

Section: Signaling Pathways Regulated By Uca1mentioning

confidence: 99%

Regulatory role of long non‑coding RNA UCA1 in signaling pathways and its clinical applications (Review)

et al. 2021

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Long non-coding RNA metastasis-associated urothelial carcinoma associated 1 (UCA1) plays a pivotal role in various human diseases. Its gene expression is regulated by several factors, including transcription factors, chromatin remodeling and epigenetic modification. UCA1 is involved in the regulation of the PI3K/AKT, Wnt/β-catenin, MAPK, NF-κB and JAK/STAT signaling pathways, affecting a series of cellular biological functions, such as cell proliferation, apoptosis, migration, invasion and tumor drug resistance. Furthermore, UCA1 is used as a novel potential biomarker for disease diagnosis and prognosis, as well as a target for clinical gene therapy. The present review systematically summarizes and elucidates the mechanisms of upstream transcriptional regulation of UCA1, the regulatory role of UCA1 in multiple signaling pathways in the occurrence and development of several diseases, and its potential applications in clinical treatment. Contents1. Introduction 2. Overview of UCA1 3. Upstream regulation of UCA1 expression 4. Signaling pathways regulated by UCA1 5. Clinical applications of UCA1 6. Conclusions and perspective

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E2F7−EZH2 axis regulates PTEN/AKT/mTOR signalling and glioblastoma progression

Cited by 61 publications

References 49 publications

POU2F2 regulates glycolytic reprogramming and glioblastoma progression via PDPK1-dependent activation of PI3K/AKT/mTOR pathway

POU2F2 regulates glycolytic reprogramming and glioblastoma progression via PDPK1-dependent activation of PI3K/AKT/mTOR pathway

MiR-365a-3p-Mediated Regulation of HELLS/GLUT1 Axis Suppresses Aerobic Glycolysis and Gastric Cancer Growth

Regulatory role of long non‑coding RNA UCA1 in signaling pathways and its clinical applications (Review)

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