IKBKE promotes glioblastoma progression by establishing the regulatory feedback loop of IKBKE/YAP1/miR-Let-7b/i

Zhang, Zhimeng; Lü, Jie; Guo, Gaochao; Yang, Yi; Dong, Shicai; Yang, Liu; Yang, Nan; Zhong, Yue; Yu, Kai; Huang, Qiang

doi:10.1177/1010428317705575

Cited by 9 publications

(6 citation statements)

References 40 publications

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“…. IKKε was found to be upregulated aberrantly in breast cancer, ovarian cancer, and GBM . Therefore, IKKε inhibition is a desirable GBM therapeutic strategy as evidenced by abundance of researches .…”

Section: Introductionmentioning

confidence: 99%

MCCK1 enhances the anticancer effect of temozolomide in attenuating the invasion, migration and epithelial‐mesenchymal transition of glioblastoma cells in vitro and in vivo

Liu

et al. 2019

Cancer Medicine

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Chemotherapy with temozolomide (TMZ) is the traditional treatment for glioblastoma (GBM). Nevertheless, majority of GBM patients have recurrence from resistance to the chemotherapy. Herein, we examined combinational effects of MCCK1 (a specific and effective IKKε inhibitor) with TMZ in GBM U251MG and U‐87MG cell lines as well as U251MG xenograft models to overcome the therapeutic limitation of chemotherapy for GBM. Although MCCK1 alone showed inhibitory effects on in vitro proliferation, migration, invasion, and EMT of U251MG and U‐87MG cells, combination of MCCK1 and TMZ showed enhanced inhibitory effects. In the U251MG GBM xenograft models, MCCK1 showed synergistic therapeutic effects in combination with TMZ to reduce tumor volumes significantly. These data indicated that MCCK1 could be a candidate sensitizer to potentiate therapeutic effects of conventional cytotoxic treatment for GBM.

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Section: Introductionmentioning

confidence: 99%

MCCK1 enhances the anticancer effect of temozolomide in attenuating the invasion, migration and epithelial‐mesenchymal transition of glioblastoma cells in vitro and in vivo

Liu

et al. 2019

Cancer Medicine

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“…A previous study by Yeom et al (4) indicated that the expression of the guanosine-5′-triphosphate-binding protein Ras related glycolysis inhibitor and calcium channel regulator is correlated with temozolomide resistance, and contributes to the poor survival of patients with GBM. The inhibitor of nuclear factor κ-B kinase subunit ε (IKBKE) is overexpressed in human GBM, and the inhibition of IKBKE markedly suppresses the proliferative and invasive activity of GBM cells (5). High expression levels of hypoxia-inducible factor-1α promote the activation of glioma cell motility by affecting molecules associated with invasion (6).…”

Section: Introductionmentioning

confidence: 99%

Identification of hub genes and pathways in glioblastoma by bioinformatics analysis

Yang

Gao

2018

Oncol Lett

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Glioblastoma (GBM) is the most common type of malignant brain tumor, and is associated with poor patient prognosis. A comprehensive understanding of the molecular mechanism underlying GBM may help to guide the identification of novel diagnoses and treatment targets. The gene expression profile of the GSE4290 GBM dataset was analyzed in order to identify differentially expressed genes (DEGs). Enriched pathways were identified through Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes analyses. A protein-protein interaction network was constructed in order to identify hub genes and for module analysis. Expression and survival analyses were conducted in order to screen and validate critical genes. A total of 1,801 DEGs were recorded, including 620 upregulated and 1,181 downregulated genes. Upregulated DEGs were enriched in the terms ‘mitotic cell cycle process’, ‘mitotic cell cycle’ and ‘cell cycle process’. Downregulated genes were enriched in ‘transsynaptic signaling’, ‘anterograde transsynaptic signaling’ and ‘synaptic signaling’. A total of 15 hub genes, which displayed a high degree of connectivity, were selected. These genes included vascular endothelial growth factor A, cyclin-dependent kinase 1 (CDK1), cell-division cycle protein 20 (CDC20), aurora kinase A (AURKA), and budding uninhibited by benzimidazoles 1 (BUB1). The identified DEGs and hub genes may help guide investigations on the mechanisms underlying the development and progression of GBM. CDK1, CDC20, AURKA and BUB1, which are involved in cell cycle pathways, may be potential targets in the diagnosis and therapy of GBM.

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“…Studies have verified that miR-155 is involved in the negative-feedback loop through downregulation of IKKε, IKKβ and other transcription factor of NF-κB [41]. Additionally, building the regulatory feedback loop of IKBKε/YAP1/miR-Let-7b/I, IKKε promotes glioblastoma progression 42 …”

Section: Introductionmentioning

confidence: 94%

“…[41] Additionally, building the regulatory feedback loop of IKBKε/YAP1/miR-Let-7b/I, IKKε promotes glioblastoma progression. 42 MyD88 and miRNAs d'Adhemar et al 43 found that miR-146a and miR-21 bind to the mRNA of MyD88 in ovarian cancer, influencing the regulatory function of MyD88 in the TLR4 pathway, whose activation does not directly promote the activation of downstream NF-kB. Meanwhile, they found that the regulatory function of miR-146a and miR-21 on MyD88 is not only limited in activating the TLR4 and NF-kB pathways, but also in regulating the expression level of MyD88 to directly influence the sensitivity of ovarian cancer cells to pharmacotherapy.…”

Section: Ikb and Mirnasmentioning

confidence: 99%

Nuclear Factor κB Signaling and Its Related Non-coding RNAs in Cancer Therapy

Liu

Shao

Zhou

et al. 2020

Molecular Therapy - Nucleic Acids

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Nuclear factor κB (NF-κB) acts as a nuclear factor that is composed of five main subunits. It is a pluripotent and crucial dimer transcription factor that has a close relationship with many serious illnesses, especially its influences on cell proliferation, inflammation, and cancer initiation and progression. NF-κB acts as part of the signaling pathway and determines its effect on the expression of several other genes, such as epidermal growth factor receptor (EGFR), p53, signal transducer and activator of transcription 3 (STAT3), and non-coding RNA (ncRNA). Continuous activation of the NF-κB signaling pathway has been seen in many cancer types. While the NF-κB signaling pathway is tightly regulated in physiological settings, quite frequently it is constitutively activated in cancer, and the molecular biology mechanism underlying the deregulated activation of NF-κB signaling remains unclear. In this review, we discuss the regulatory role and possible clinical significance of ncRNA (microRNA [miRNA] and long non-coding RNA [lncRNA]) in NF-κB signaling in cancer, including in the conversion of inflammation to carcinogenesis. Non-coding RNA plays an essential and complex role in the NF-κB signaling pathway. NF-κB activation can also induce the ncRNA status. Targeting NF-κB signaling by ncRNA is becoming a promising strategy of drug development and cancer treatment.

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IKBKE promotes glioblastoma progression by establishing the regulatory feedback loop of IKBKE/YAP1/miR-Let-7b/i

Cited by 9 publications

References 40 publications

MCCK1 enhances the anticancer effect of temozolomide in attenuating the invasion, migration and epithelial‐mesenchymal transition of glioblastoma cells in vitro and in vivo

MCCK1 enhances the anticancer effect of temozolomide in attenuating the invasion, migration and epithelial‐mesenchymal transition of glioblastoma cells in vitro and in vivo

Identification of hub genes and pathways in glioblastoma by bioinformatics analysis

Nuclear Factor κB Signaling and Its Related Non-coding RNAs in Cancer Therapy

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