ArticleCancer research2008
Nitrosoureas inhibit the stathmin-mediated migration and invasion of malignant glioma cells.
Article in Cancer research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
14 citing papers in PubMed, 34 citations in OpenAlex.
- Crude Venom from Sea AnemoneMarine drugs · 2026Article
- Mitochondria-targeted Re(I) complexes bearing guanidinium as ligands and their anticancer activity.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2020Article
- Zyxin (ZYX) promotes invasion and acts as a biomarker for aggressive phenotypes of human glioblastoma multiforme.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- PHAP1 promotes glioma cell proliferation by regulating the Akt/p27/stathmin pathway.Journal of cellular and molecular medicine · 2018Article
- MYCN and HDAC5 transcriptionally repress CD9 to trigger invasion and metastasis in neuroblastoma.Oncotarget · 2016Article
- Stathmin in pancreatic neuroendocrine neoplasms: a marker of proliferation and PI3K signaling.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- MicroRNA-9 inhibits vasculogenic mimicry of glioma cell lines by suppressing Stathmin expression.Journal of neuro-oncology · 2013Article
- Stathmin and microtubules regulate mitotic entry in HeLa cells by controlling activation of both Aurora kinase A and Plk1.Molecular biology of the cell · 2013Article
- Discovery of structural alterations in solid tumor oligodendroglioma by single molecule analysis.BMC genomics · 2013Article
- Endosomolytic anionic polymer for the cytoplasmic delivery of siRNAs in localizedAdvanced functional materials · 2013Article
- MicroRNA-195 plays a tumor-suppressor role in human glioblastoma cells by targeting signaling pathways involved in cellular proliferation and invasion.Neuro-oncology · 2012Article
- Neurological surgery at the National Institutes of Health.World neurosurgery · 2010Article
- Antigen-specific T-cell response from dendritic cell vaccination using cancer stem-like cell-associated antigens.Stem cells (Dayton, Ohio) · 2009Article
- Current concepts in the evaluation and management of WHO grade II gliomas.Journal of neuro-oncology · 2009Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Malignant gliomas are the most common primary intrinsic brain tumors and are highly lethal. The widespread migration and invasion of neoplastic cells from the initial site of tumor formation into the surrounding brain render these lesions refractory to definitive surgical treatment. Stathmin, a microtubule-destabilizing protein that mediates cell cycle progression, can also regulate directed cell movement. Nitrosoureas, traditionally viewed as DNA alkylating agents, can also covalently modify proteins such as stathmin. We therefore sought to establish a role for stathmin in malignant glioma cell motility, migration, and invasion and determine the effects of nitrosoureas on these cell movement-related processes. Scratch wound-healing recovery, Boyden chamber migration, Matrigel invasion, and organotypic slice invasion assays were performed before and after the down-regulation of cellular stathmin levels and in the absence and presence of sublethal nitrosourea ([1-(2-chloroethyl)-3-cyclohexyl-l-nitrosourea]; CCNU) concentrations. We show that decreases in stathmin expression lead to significant decreases in malignant glioma cell motility, migration, and invasion. CCNU, at a concentration of 10 micromol/L, causes similar significant decreases, even in the absence of any effects on cell viability. The direct inhibition of stathmin by CCNU is likely a contributing factor. These findings suggest that the inhibition of stathmin expression and function may be useful in limiting the spread of malignant gliomas within the brain, and that nitrosoureas may have therapeutic benefits in addition to their antiproliferative effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.