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Related Experiment Video

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Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

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p38MAPK activation and DUSP10 expression in meningiomas.

Mahlon D Johnson¹, Jay E Reeder², Mary O'Connell¹

¹Department of Pathology, Division of Neuropathology, University of Rochester Medical Center, 601 Elmwood Avenue, Box 626, Rochester, NY 14623, USA.

Journal of Clinical Neuroscience : Official Journal of the Neurosurgical Society of Australasia

|April 7, 2016

Summary

Mitogen-activated protein kinase (MAPK) p38MAPK and dual-specificity phosphatase 10 (DUSP10) are involved in meningioma cell growth. DUSP10 expression inversely correlates with p38MAPK phosphorylation in most meningiomas, suggesting a role in tumor development.

Keywords:

DUSP10 Leptomeninges Meningioma Phosphatases p38MAPK p44/42MAPK

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Area of Science:

Oncology
Molecular Biology
Cell Signaling

Background:

Mitogen-activated protein kinase (MAPK) p38MAPK is crucial for cell proliferation and apoptosis.
The role of p38MAPK, its activation, and regulation by dual-specificity phosphatases (DUSP), specifically DUSP10, in meningiomas remains uncharacterized.
DUSP10 is a potential regulator of meningioma cell proliferation.

Purpose of the Study:

To investigate the expression, activation, and regulation of DUSP10 and p38MAPK signaling in human meningiomas.
To explore the in vitro effects of platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor B1 (TGFB1) on DUSP10 and MAPK signaling in meningioma cultures.

Main Methods:

Western blot analysis was used to detect DUSP10 and phosphorylated p38MAPK and p44/42MAPK.
Polymerase chain reaction (PCR) was employed to assess DUSP10 expression.
In vitro studies examined the effects of PDGF-BB, TGFB1, and cerebrospinal fluid on meningioma cells.

Main Results:

DUSP10 and phosphorylated p38MAPK/p44/42MAPK were present in normal leptomeninges and meningiomas across all World Health Organization grades.
DUSP10 expression generally showed an inverse correlation with p38MAPK phosphorylation in meningiomas.
PDGF-BB upregulated DUSP10, while TGFB1 increased p38MAPK phosphorylation and caspase 3 activation.

Conclusions:

p38MAPK and DUSP10 are likely involved in the pathogenesis of meningiomas.
The interplay between DUSP10 and p38MAPK signaling pathways may represent a therapeutic target for meningioma treatment.