Impact of meriolins, a new class of cyclin-dependent kinase inhibitors, on malignant glioma proliferation and neo-angiogenesis

Jarry, Marie; Lecointre, Céline; Malleval, Céline; Desrues, Laurence; Schouft, Marie‐Thérèse; Lejoncour, Vadim; Mouton-Liger, François; Lyvinec, Gildas; Joseph, Benoı̂t; Loaëc, Nadège; Meijer, Laurent; Honnorat, Jérôme; Gandolfo, Pierrick; Castel, Hélène

doi:10.1093/neuonc/nou102

Cited by 28 publications

(47 citation statements)

References 60 publications

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“…GBM xenograft growth was evaluated after subcutaneous (s.c.) injection, into the flank of 4-week-old male nude mice, of GBM xenografts (GBM_SC1 or GBM_SC2) as described previously (30). When the first tumor reached the size of approximately 1,500 mm 3 , mice were euthanized.…”

Section: Xenograft Transplantation In Micementioning

confidence: 99%

CRMP5 Controls Glioblastoma Cell Proliferation and Survival through Notch-Dependent Signaling

et al. 2015

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Collapsin response mediator protein 5 (CRMP5) belongs to a family of five cytosolic proteins that play a major role in nervous system development. This protein was first described in cancerinduced autoimmune processes, causing neurodegenerative disorders (paraneoplastic neurologic syndromes). CRMP5 expression has been reported to serve as a biomarker for high-grade lung neuroendocrine carcinomas; however, its functional roles have not been examined in any setting of cancer pathophysiology. In this study, we report two different CRMP5 expression patterns observed in human glioblastoma (GBM) biopsies that establish connections between CRMP5 expression, Notch receptor signaling, and GBM cell proliferation. We demonstrated that elevated CRMP5 promotes Notch receptor expression and Akt activation in human tumor cell lines, GBM stem cells, and primary tumor biopsies. We have shown that the high CRMP5 and Notch expression in GBM xenograft is related to stem cells. This suggests that high CRMP5 expression pattern in GBM biopsies encompasses a subset of stem cells. Mechanistically, CRMP5 functioned by hijacking Notch receptors from Itch-dependent lysosomal degradation. Our findings suggest that CRMP5 serves as a major mediator of Notch signaling and Akt activation by controlling the degradation of the Notch receptor, with implications for defining a biomarker signature in GBM that correlates with and may predict patient survival. Cancer Res; 75(17); 3519-28. Ó2015 AACR.

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Section: Xenograft Transplantation In Micementioning

confidence: 99%

CRMP5 Controls Glioblastoma Cell Proliferation and Survival through Notch-Dependent Signaling

et al. 2015

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“…Selectivity of expressed transmembrane proteins across the BBB enhanced the cross-membrane transport and delivery to active sites in human neuroglioma. However, increased adenosine triphosphate ATP in human H4 neuroglioma cells increased alpha synuclein, and inhibited neurogenesis [15]. Intracellular protein expression of meriolins on arctic medicinal marine invertebrates inhibited cyclin-dependent kinase, decreased ATP [16].…”

Section: Resultsmentioning

confidence: 99%

Medicinal Plant and Anticancer Activity on Neuroglioma

Shivers

Yedjou²,

Mbemi³

et al. 2017

IJMSCI

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This document file is a live template. The various components of your paper [title, text, heads, etc.] are exactly defined on the style sheet, as illustrated by the portions given in this document. Do not include any special characters, symbols, or math in your title or abstract. The authors must follow the guidelines given in the document for the papers to be published. You can use this document file as both an instruction set and as a template into which you can type your own text.

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“…Recently, synthetic hybrid molecules called meriolins were derived from meridianins, and shown to induce apoptosis in neuroblatoma SH-SY5Y cells [ 141 ]. Comparative analysis of a panel of meriolins showed that meriolin-15 significantly inhibited proliferation and induced apoptosis in GBM cells [ 142 ].…”

Section: Natural Products Effecting Gbm Cell Proliferation and Apoptomentioning

confidence: 99%

Natural products: a hope for glioblastoma patients

et al. 2018

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Glioblastoma (GBM) is one of the most aggressive malignant tumors with an overall dismal survival averaging one year despite multimodality therapeutic interventions including surgery, radiotherapy and concomitant and adjuvant chemotherapy. Few drugs are FDA approved for GBM, and the addition of temozolomide (TMZ) to standard therapy increases the median survival by only 2.5 months. Targeted therapy appeared promising in in vitro monolayer cultures, but disappointed in preclinical and clinical trials, partly due to the poor penetration of drugs through the blood brain barrier (BBB). Cancer stem cells (CSCs) have intrinsic resistance to initial chemoradiation therapy (CRT) and acquire further resistance via deregulation of many signaling pathways. Due to the failure of classical chemotherapies and targeted drugs, research efforts focusing on the use of less toxic agents have increased. Interestingly, multiple natural compounds have shown antitumor and apoptotic effects in TMZ resistant and p53 mutant GBM cell lines and also displayed synergistic effects with TMZ. In this review, we have summarized the current literature on natural products or product analogs used to modulate the BBB permeability, induce cell death, eradicate CSCs and sensitize GBM to CRT.

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Impact of meriolins, a new class of cyclin-dependent kinase inhibitors, on malignant glioma proliferation and neo-angiogenesis

Abstract: Meriolins, and meriolin 15 in particular, exhibit antiproliferative and proapoptotic activities on both glioma and intratumoral endothelial cells, constituting key promising therapeutic lead compounds for the treatment of glioblastoma.

Cited by 28 publications

References 60 publications

CRMP5 Controls Glioblastoma Cell Proliferation and Survival through Notch-Dependent Signaling

CRMP5 Controls Glioblastoma Cell Proliferation and Survival through Notch-Dependent Signaling

Medicinal Plant and Anticancer Activity on Neuroglioma

Natural products: a hope for glioblastoma patients

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