CRM1/XPO1 is associated with clinical outcome in glioma and represents a therapeutic target by perturbing multiple core pathways

Liu, Xuejiao; Chong, Yulong; Tu, Yiming; Liu, Ning; Yue, Chenglong; Qi, Zhenglei; Liu, Huize; Yao, Yao; Liu, Hongmei; Gao, Shangfeng; Niu, Mingshan; Yu, Rutong

doi:10.1186/s13045-016-0338-2

Cited by 57 publications

(58 citation statements)

References 43 publications

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“…Immunofluorescence and Western blotting were done as described previously . Antibodies against S100A11(ab180593), Cyclin D1(ab40754), Cyclin E1 (ab33911), Cleaved caspase‐3 (ab13585), Bcl‐2 (ab32124), Bax (ab32503), p‐IKKα (Thr23, ab38515) and Fibronectin (ab2413, Abcam); E‐cadherin (#3195), CD133 (#64326), Nestin (#33475), N‐cadherin (#13116), Nanog (#4903), Oct4 (#75463), Vimentin (#5741), ANXA2 (#8235), HA (#5017), Myc (#2276), Histone H3 (#4499), Actin (#3700), GAPDH (#5174), IκBα (#4814), IKKα (#11930), p65 (#8242) and p‐p65 (#3033, Cell Signaling Technology) were used for immunofluorescence and Western blotting.…”

Section: Methodsmentioning

confidence: 99%

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S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop

Xie

et al. 2019

J Cellular Molecular Medi

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Glioblastoma (GBM) is the most universal type of primary brain malignant tumour, and the prognosis of patients with GBM is poor. S100A11 plays an essential role in tumour. However, the role and molecular mechanism of S100A11 in GBM are not clear. Here, we found that S100A11 was up‐regulated in GBM tissues and higher S100A11 expression indicated poor prognosis of GBM patients. Overexpression of S100A11 promoted GBM cell growth, epithelial‐mesenchymal transition (EMT), migration, invasion and generation of glioma stem cells (GSCs), whereas its knockdown inhibited these activities. More importantly, S100A11 interacted with ANXA2 and regulated NF‐κB signalling pathway through decreasing ubiquitination and degradation of ANXA2. Additionally, NF‐κB regulated S100A11 at transcriptional level as a positive feedback. We also demonstrated the S100A11 on tumour growth in GBM using an orthotopic tumour xenografting. These data demonstrate that S100A11/ANXA2/NF‐κB positive feedback loop in GBM cells that promote the progression of GBM.

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Section: Methodsmentioning

confidence: 99%

“…Immunofluorescence and Western blotting were done as described previously. 18 Antibodies against S100A11(ab180593),…”

Section: Immunofluorescence and Western Blottingmentioning

confidence: 99%

S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop

Xie

et al. 2019

J Cellular Molecular Medi

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“…Lenti-RASD1 or Lenti-Vector U87 cells (1 × 10 6 ) were stereotactically injected into the right striatum of nude mice as described in our previous studies 30, 31 . The mice were sacrificed when cachexia occurred in the tumor growth assay or at two weeks after glioma cell transplantation for the tumor invasion assay.…”

Section: Methodsmentioning

confidence: 99%

Overexpression of RASD1 inhibits glioma cell migration/invasion and inactivates the AKT/mTOR signaling pathway

Gao

Jin

Liu

et al. 2017

Sci Rep

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The RAS signaling pathway is hyperactive in malignant glioma due to overexpression and/or increased activity. A previous study identified that RASD1, a member of the RAS superfamily of small G-proteins, is a significantly dysregulated gene in oligodendroglial tumors that responded to chemotherapy. However, the role and mechanism of RASD1 in the progression of human glioma remain largely unknown. In the present study, by analyzing a public genomics database, we found that high levels of RASD1 predicted good survival of astrocytoma patients. We thus established lentivirus-mediated RASD1-overexpressing glioma cells and found that overexpressing RASD1 had no significant effects on glioma cell proliferation. However, the overexpression of RASD1 inhibited glioma cell migration and invasion. In the intracranial glioma xenograft model, the overexpression of RASD1 significantly reduced the number of tumor cells invading into the surrounding tissues without affecting the tumor size. An intracellular signaling array revealed that the phosphorylation of both AKT and the S6 ribosomal protein significantly decreased with RASD1 overexpression in glioma cells. Interestingly, RASD1 protein levels were significantly higher in grade II and grade III astrocytoma tissues than in nontumorous brain tissues. These findings suggest that the upregulation of RASD1 in glioma tissues may play an inhibitory role in tumor expansion, possibly through inactivating the AKT/mTOR signaling pathway.

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“…GBM has more pronounced malignant features, including uncontrolled cellular proliferation, increased angiogenesis, and resistance to apoptosis [1][2][3]. Therefore, patients diagnosed with GBM have a very poor prognosis with an average survival of 12-15 months post diagnosis [4,5].…”

Section: Introductionmentioning

confidence: 99%

The Role of Rho GTPases in Motility and Invasion of Glioblastoma Cells

Al-Koussa

Atat

Jaafar

et al. 2020

Analytical Cellular Pathology

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Astrocytomas are primary malignant brain tumors that originate from astrocytes. Grade IV astrocytoma or glioblastoma is a highly invasive tumor that occur within the brain parenchyma. The Rho family of small GTPases, which includes Rac1, Cdc42, and RhoA, is an important family whose members are key regulators of the invasion and migration of glioblastoma cells. In this review, we describe the role played by the Rho family of GTPases in the regulation of the invasion and migration of glioblastoma cells. Specifically, we focus on the role played by RhoA, Rac1, RhoG, and Cdc42 in cell migration through rearrangement of actin cytoskeleton, cell adhesion, and invasion. Finally, we highlight the importance of potentially targeting Rho GTPases in the treatment of glioblastoma.

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CRM1/XPO1 is associated with clinical outcome in glioma and represents a therapeutic target by perturbing multiple core pathways

Cited by 57 publications

References 43 publications

S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop

S100A11 functions as novel oncogene in glioblastoma via S100A11/ANXA2/NF‐κB positive feedback loop

Overexpression of RASD1 inhibits glioma cell migration/invasion and inactivates the AKT/mTOR signaling pathway

The Role of Rho GTPases in Motility and Invasion of Glioblastoma Cells

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