RETRACTED ARTICLE: MYC-mediated upregulation of PNO1 promotes
glioma tumorigenesis by activating THBS1/FAK/Akt signaling

Chen, Xu; Guo, Zheng-Qian; Cao, Dan; Chen, Yong; Chen, Jian

doi:10.1038/s41419-021-03532-y

Cited by 21 publications

(12 citation statements)

References 44 publications

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“…S4D ). AKT and ERK1/2 were downstream mediators of FAK pathway, and FAK/AKT/ERK1/2 axis is one of the focal adhesion pathways that are important for cell proliferation and motility [ 25 , 26 ]. Immunoblot findings revealed that p-AKT (Ser473) and p-ERK1/2(Thr202/Tyr204) proteins expression were obviously decreased in MEOX2 knockdown cells, while were significantly increased in MEOX2 overexpression cells (Fig.…”

Section: Resultsmentioning

confidence: 99%

MEOX2-mediated regulation of Cathepsin S promotes cell proliferation and motility in glioma

Chen

Wang

et al. 2022

Cell Death Dis

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Nuclear transcription factor Mesenchyme Homeobox 2 (MEOX2) is a homeobox gene that is originally discovered to suppress the growth of vascular smooth muscle and endothelial cells. However, whether or not it is connected to cancer is yet unknown. Here, we report that MEOX2 functions as a tumor-initiating element in glioma. Bioinformatic analyses of public databases and investigation of MEOX2 expression in patients with glioma demonstrated that MEOX2 was abundant at both mRNA and protein levels in glioma. MEOX2 expression was shown to be inversely linked with the prognosis of glioma patients. MEOX2 inhibition changed the morphology of glioma cells, inhibited cell proliferation and motility, whereas had no effect on cell apoptosis. Besides, silencing MEOX2 also hampered the epithelial-mesenchymal transition (EMT), focal adhesion formation, and F-actin assembly. Overexpression of MEOX2 exhibited opposite effects. Importantly, RNA-sequencing, ChIP-qPCR assay, and luciferase reporter assay revealed Cathepsin S (CTSS) as a novel transcriptional target of MEOX2 in glioma cells. Consistently, MEOX2 causes glioma tumor development in mice and greatly lowers the survival period of tumor-bearing mice. Our findings indicate that MEOX2 promotes tumorigenesis and progression of glioma partially through the regulation of CTSS. Targeting MEOX2-CTSS axis might be a promising alternative for the treatment of glioma.

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Section: Resultsmentioning

confidence: 99%

MEOX2-mediated regulation of Cathepsin S promotes cell proliferation and motility in glioma

Chen

Wang

et al. 2022

Cell Death Dis

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“…Bromodomain-4 protein (BRD4) positively regulates EZH2 transcription through Myc upregulation [ 56 ]. Myc activation was reported in glioblastoma progression, particularly in poor prognosis and therapy resistant-tumors [ 55 , 57 ]. EZH2 mediates proliferation, migration, and invasion in GBM.…”

Section: Discussionmentioning

confidence: 99%

EZH2-Myc driven glioblastoma elicited by cytomegalovirus infection of human astrocytes

et al. 2023

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Mounting evidence is identifying human cytomegalovirus (HCMV) as a potential oncogenic virus. HCMV has been detected in malignant gliomas. EZH2 and Myc play a potential oncogenic role, correlating with the glioma grade. Herewith, we present the first experimental evidence for HCMV as a reprogramming vector, straight through the dedifferentiation of mature human astrocytes, and generation of CMV-Elicited Glioblastoma Cells (CEGBCs) possessing glioblastoma-like traits. HCMV counterparts the progression of the perceived cellular and molecular mechanisms succeeding the transformation and invasion processes with CEGBCs involved in spheroid formation and invasiveness. Glioblastoma multiforme (GBM) biopsies were characterized by an elevated EZH2 and Myc expression, possessing a strong positive correlation between the aforementioned markers in the presence of HCMV. From GBM tissues, we isolated HCMV clinical strains that transformed HAs toward CEGBCs exhibiting upregulated EZH2 and Myc. Spheroids generated from CEGBCs possessed invasion potential and were sensitive to EZH2 inhibitor, ganciclovir, and temozolomide triple therapy. HCMV clinical strains transform HAs and fit with an HCMV-induced glioblastoma model of oncogenesis, and supports the tumorigenic properties of Myc and EZH2 which might be highly pertinent in the pathophysiology of astrocytic brain tumors and thereby paving the way for new therapeutic strategies.

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“…In this study, besides THBS1, DDIT4, TCL1A, and AREG might be biological markers in the prognosis of septic shock by acting via PI3K/Akt signaling pathway. Still, the role of THBS1 in the regulation of the PI3K-Akt signaling pathway in cancer is relatively well defined [34], but its role in sepsis remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Identification of transcriptomics biomarkers for the early prediction of the prognosis of septic shock from pneumopathies

et al. 2021

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Background Identifying the biological subclasses of septic shock might provide specific targeted therapies for the treatment and prognosis of septic shock. It might be possible to find biological markers for the early prediction of septic shock prognosis. Methods The data were obtained from the Gene Expression Omnibus databases (GEO) in NCBI. GO enrichment and KEGG pathway analyses were performed to investigate the functional annotation of up- and downregulated DEGs. ROC curves were drawn, and their areas under the curves (AUCs) were determined to evaluate the predictive value of the key genes. Results 117 DEGs were obtained, including 36 up- and 81 downregulated DEGs. The AUC for the MME gene was 0.879, as a key gene with the most obvious upregulation in septic shock. The AUC for the THBS1 gene was 0.889, as a key downregulated gene with the most obvious downregulation in septic shock. Conclusions The upregulation of MME via the renin-angiotensin system pathway and the downregulation of THBS1 through the PI3K–Akt signaling pathway might have implications for the early prediction of prognosis of septic shock in patients with pneumopathies.

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RETRACTED ARTICLE: MYC-mediated upregulation of PNO1 promotes glioma tumorigenesis by activating THBS1/FAK/Akt signaling

Cited by 21 publications

References 44 publications

MEOX2-mediated regulation of Cathepsin S promotes cell proliferation and motility in glioma

MEOX2-mediated regulation of Cathepsin S promotes cell proliferation and motility in glioma

EZH2-Myc driven glioblastoma elicited by cytomegalovirus infection of human astrocytes

Identification of transcriptomics biomarkers for the early prediction of the prognosis of septic shock from pneumopathies

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