Primary brain tumours in adults

Béhin, Anthony; Hoang-Xuân, Khê; Carpentier, Antoine F.; Delattre, Jean‐Yves

doi:10.1016/s0140-6736(11)61346-9

Cited by 719 publications

(444 citation statements)

References 127 publications

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“…Malignant gliomas are highly aggressive, angiogenic, and incurable tumors that exhibit a mortality rate higher than any other brain malignancy [1] . Glioma treatment, including surgery, radiotherapy, and chemotherapy, remains a challenging issue [2] .…”

Section: Introductionmentioning

confidence: 99%

Probucol suppresses human glioma cell proliferation in vitro via ROS production and LKB1-AMPK activation

et al. 2014

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Aim: Probucol, an anti-hyperlipidemic drug, has been reported to exert antitumor activities at various stages of tumor initiation, promotion and progression. In this study we examined whether the drug affected glioma cell growth in vitro and the underlying mechanisms. Methods: Human glioma U87 and glioblastoma SF295 cell lines were used. Cell proliferation was accessed using the cell proliferation assay and BrdU incorporation. The phosphorylation of AMPK, liver kinase B1 (LKB1) and p27 Kip1 was detected by Western blot. The activity of 26S proteasome was assessed with an in situ fluorescent substrate. siRNAs were used to suppress the expression of the relevant signaling proteins. Results: Treatment of U87 glioma cells with probucol (10-100 μmol/L) suppressed the cell proliferation in dose-and time-dependent manners. Meanwhile, probucol markedly increased the ROS production, phosphorylation of AMPK at Thr172 and LKB1 at Ser428 in the cells. Furthermore, probucol significantly decreased 26S proteasome activity and increased p27 Kip1 protein level in the cells in an AMPK-dependent manner. Probucol-induced suppression of U87 cell proliferation could be reversed by pretreatment with tempol (a superoxide dismutase mimetic), MG132 (proteasome inhibitor) or compound C (AMPK inhibitor), or by gene silencing of LKB1, AMPK or p27 Kip1 . Similar results were observed in probucol-treated SF295 cells. Conclusion: Probucol suppresses human glioma cell proliferation in vitro via ROS production and LKB1-AMPK activation, which reduces 26S proteasome-dependent degradation of p27 Kip1 .

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Section: Introductionmentioning

confidence: 99%

Probucol suppresses human glioma cell proliferation in vitro via ROS production and LKB1-AMPK activation

et al. 2014

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“…The most malignant type of glioma is glioblastoma (1). Although glioma can be treated by comprehensive regimens, including postoperative radiotherapy in combination with temozolomide chemotherapy, excessive glioma cell proliferation, apoptotic resistance, advanced invasion and infiltration, and chemotherapeutic drug resistance can result in unsatisfactory treatment outcomes.…”

Section: Introductionmentioning

confidence: 99%

miR-130b regulates the proliferation, invasion and apoptosis of glioma cells via targeting of CYLD

Xiao

Yin

et al. 2017

Oncology Reports

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Abstract. MicroRNAs are short non-coding RNAs that play important roles in gliomas. However, the role of miR-130b in glioma remains unclear. In the present study, miR-130b expression was upregulated in glioma tissues and cell lines. Kaplan-Meier analysis indicated that the upregulation of miR-130b expression correlated with poor prognoses in glioma patients. Multivariate analysis demonstrated that this upregulation and a high-grade classification were independent factors that both predicted poor outcomes for glioma patients. Dual-luciferase assays identified that the cylindromatosis (CYLD) gene is a direct target of miR-130b. Functional studies demonstrated that a miR-130b mimic significantly promoted the growth and invasion of glioma cells, while also inhibiting apoptosis via selective targeting of CYLD, which was enhanced by CYLD-targeted siRNA. In contrast, a miR-130b inhibitor suppressed these biological behaviors, and this inhibition was reversed by CYLD-targeted siRNA. These data revealed that miR-130b could act as a novel potential diagnostic biomarker for glioma, while also demonstrating the importance of miR-130b in the cell proliferation and progression of glioma, indicating that it may serve as a useful therapeutic target for glioma.

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“…1 Surgery followed by radiotherapy and temozolomide-based chemotherapy represents the current standard of care for patients and modestly improves their median survival. 2 Moreover, rapid tumor relapse often takes place in the vicinity of the resected tumor 3 and could be attributed to a high molecular/cellular heterogeneity in GBM combined with a diffuse and deep invasion of highly radio-and chemoresistant cell subsets, 4,5 called cancer stem cells (CSC), which share phenotypic features with normal stem cells.…”

Section: Introductionmentioning

confidence: 99%

Stereotaxic administrations of allogeneic human Vγ9Vδ2 T cells efficiently control the development of human glioblastoma brain tumors

et al. 2016

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Primary brain tumours in adults

Cited by 719 publications

References 127 publications

Probucol suppresses human glioma cell proliferation in vitro via ROS production and LKB1-AMPK activation

Probucol suppresses human glioma cell proliferation in vitro via ROS production and LKB1-AMPK activation

miR-130b regulates the proliferation, invasion and apoptosis of glioma cells via targeting of CYLD

Stereotaxic administrations of allogeneic human Vγ9Vδ2 T cells efficiently control the development of human glioblastoma brain tumors

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