Abnormal regulation of mammalian p21ras contributes to malignant tumor growth in von Recklinghausen (type 1) neurofibromatosis

DeClue, Jeffrey E.; Papageorge, Alex G.; Fletcher, Jonathan A.; Diehl, Scott R.; Ratner, Nancy; Vass, William C.; Lowy, Douglas R.

doi:10.1016/0092-8674(92)90407-4

Cited by 580Neurofibromatosis and Schwannoma CasesProtein Kinase Regulation and GTPase SignalingProtein Tyrosine Phosphatases

Abnormal regulation of mammalian p21ras contributes to malignant tumor growth in von Recklinghausen (type 1) neurofibromatosis

DeClue, Jeffrey E., Papageorge, Alex G., Fletcher, Jonathan A., Diehl, Scott R., Ratner, Nancy, Vass, William C., Lowy, Douglas R.·1992·Cell

DOI 10.1016/0092-8674(92)90407-4

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Abstract

Tumor cell lines derived from malignant schwannomas removed from patients with neurofibromatosis type 1 (NF1) have been examined for the level of expression of NF1 protein. All three NF1 lines examined expressed lower levels of NF1 protein than control cells, and the level in one line was barely detectable. The tumor lines expressed normal levels of p120GAP and p21ras. Although the p21ras proteins isolated from the tumor cells had normal (nonmutant) biochemical properties in vitro, they displayed elevated levels of bound GTP in vivo. The level of total cellular GAP-like activity was reduced in extracts from the tumor line that expresses very little NF1 protein. Introduction of the catalytic region of GAP into this line resulted in morphological reversion and lower in vivo GTP binding by endogenous p21ras. These data implicate NF1 protein as a tumor suppressor gene product that negatively regulates p21ras and define a "positive" growth role for ras activity in NF1 malignancies.

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Supplementary Figure 1 from Phenotypic Reversion of Invasive Neurofibromin-Deficient Schwannoma by FTS: Ras Inhibition Reduces BMP4/Erk/Smad Signaling
Barkan, B., Kloog, Y., & Ehrlich, M. (2023) · doi:10.1158/1535-7163.22497091.v1
Supplementary Figure 2 from Phenotypic Reversion of Invasive Neurofibromin-Deficient Schwannoma by FTS: Ras Inhibition Reduces BMP4/Erk/Smad Signaling
Barkan, B., Kloog, Y., & Ehrlich, M. (2023) · doi:10.1158/1535-7163.22497088
Supplementary Figure 3 from Phenotypic Reversion of Invasive Neurofibromin-Deficient Schwannoma by FTS: Ras Inhibition Reduces BMP4/Erk/Smad Signaling
Barkan, B., Kloog, Y., & Ehrlich, M. (2023) · doi:10.1158/1535-7163.22497085.v1
Supplementary Figure 4 from Phenotypic Reversion of Invasive Neurofibromin-Deficient Schwannoma by FTS: Ras Inhibition Reduces BMP4/Erk/Smad Signaling
Barkan, B., Kloog, Y., & Ehrlich, M. (2023) · doi:10.1158/1535-7163.22497082
Supplementary Figure 4 from Phenotypic Reversion of Invasive Neurofibromin-Deficient Schwannoma by FTS: Ras Inhibition Reduces BMP4/Erk/Smad Signaling
Barkan, B., Kloog, Y., & Ehrlich, M. (2023) · doi:10.1158/1535-7163.22497082.v1

Authors: DeClue, J. E., Papageorge, A. G., Fletcher, J. A., Diehl, S. R., Ratner, N., Vass, W. C., & Lowy, D. R.
Affiliations: National Cancer Institute (US)
Brigham and Women's Hospital (US)
Virginia Commonwealth University (US)
ORCID: Diehl, Scott R.
Ratner, Nancy
Lowy, Douglas R.
Venue: Cell
Publisher: Elsevier BV
Published: 1992-04
Volume: 69
Issue: 2
Pages: 265-273
ISSN: 0092-8674 (ISSN-L)
DOI: 10.1016/0092-8674(92)90407-4
OpenAlex: W2072478579
Cited by: 580
References: 58
Citations by year: 2026: 7 · 2025: 7 · 2024: 7 · 2023: 10 · 2022: 8 · 2021: 5 · 2020: 10 · 2019: 10 · 2018: 4 · 2017: 4 · 2016: 14 · 2015: 12 · 2014: 21 · 2013: 17 · 2012: 18
FWCI: 35.71
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Cell (publishedVersion)
PubMed (publishedVersion)
Funders: National Cancer Institute (CA 16059, P30CA016059)
Topics: Health Sciences › Medicine › Neurology › Neurofibromatosis and Schwannoma Cases
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
Keywords: neurofibromatosis type 1, p21ras, tumor suppressor, malignant peripheral nerve sheath tumor, GTP binding, cancer cell lines, Ras signaling
MeSH terms: Animals, Guanosine Triphosphate, Humans, Neurilemmoma, Neurofibromatosis 1, Protein Binding, Proteins, Tumor Cells, Cultured, Gene Expression Regulation, Neoplastic, Genes, Tumor Suppressor, Proto-Oncogene Proteins p21(ras), Neurofibromin 1, Mice

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Abnormal regulation of mammalian p21ras contributes to malignant tumor growth in von Recklinghausen (type 1) neurofibromatosis

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