SNAI2/Slug promotes growth and invasion in human gliomas

Yang, Hong; Menon, Lata G.; Black, Peter McLaren; Carroll, Rona S.; Johnson, Mark D.

doi:10.1186/1471-2407-10-301

Cited by 134 publications

(115 citation statements)

References 27 publications

(34 reference statements)

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“…A recent report has shown that miR-124a and miR-203 play critical roles in cancers (43)(44)(45)(46)(47). Furthermore, SLUG acts as a predictive marker for the clinical outcome of patients with lung adenocarcinoma, breast, ovarian, colon, and gastric cancers (43,(48)(49)(50).…”

Section: Discussionmentioning

confidence: 99%

Angiopoietin-like protein 1 suppresses SLUG to inhibit cancer cell motility

Kuo¹,

Tan²,

Chang³

et al. 2013

J. Clin. Invest.

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Section: Discussionmentioning

confidence: 99%

Angiopoietin-like protein 1 suppresses SLUG to inhibit cancer cell motility

Kuo¹,

Tan²,

Chang³

et al. 2013

J. Clin. Invest.

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“…40,56 Snail/Slug proteins have already been involved in GBM invasion. 57,58 We demonstrate the regulation of Snail/Slug, in parallel to increased PY142 b-catenin, upon stimulation of GBM cells with HGF. Statistical studies indicate that both nuclear Snail/ Slug and nuclear PY142 b-catenin peak in astrocytomas of grade III.…”

Section: Resultsmentioning

confidence: 99%

Nuclear phosphorylated Y142 β-catenin accumulates in astrocytomas and glioblastomas and regulates cell invasion

et al. 2015

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Glioblastoma multiforme (GBM) is a fast growing brain tumor characterized by extensive infiltration into the surrounding tissue and one of the most aggressive cancers. GBM is the most common glioma (originating from glialderived cells) that either evolves from a low grade astrocytoma or appears de novo. Wnt/b-catenin and Hepatocyte Growth Factor (HGF)/c-Met signaling are hyperactive in human gliomas, where they regulate cell proliferation, migration and stem cell behavior. We previously demonstrated that b-catenin is phosphorylated at Y142 by recombinant c-Met kinase and downstream of HGF signaling in neurons. Here we studied phosphoY142 (PY142) b-catenin and dephospho S/T b-catenin (a classical Wnt transducer) in glioma biopsies, GBM cell lines and biopsyderived glioma cell cultures. We found that PY142 b-catenin mainly localizes in the nucleus and signals through transcriptional activation in GBM cells. Tissue microarray analysis confirmed strong nuclear PY142 b-catenin immunostaining in astrocytoma and GBM biopsies. By contrast, active b-catenin showed nuclear localization only in GBM samples. Western blot analysis of tumor biopsies further indicated that PY142 and active b-catenin accumulate independently, correlating with the expression of Snail/Slug (an epithelial-mesenchymal transition marker) and Cyclin-D1 (a regulator of cell cycle progression), respectively, in high grade astrocytomas and GBMs. Moreover, GBM cells stimulated with HGF showed increasing levels of PY142 b-catenin and Snail/Slug. Importantly, the expression of mutant Y142F b-catenin decreased cell detachment and invasion induced by HGF in GBM cell lines and biopsy-derived cell cultures. Our results identify PY142 b-catenin as a nuclear b-catenin signaling form that downregulates adhesion and promotes GBM cell invasion.

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“…In GBM, the Rho family GTPase (RND)-3 has been shown to promote the degradation of SNAIL in vitro and in vivo, while downregulation of RND3 strongly induces SNAIL expression and migration (166). SLUG expression was found to correlate with histologic grade and invasive phenotype in glioma, whereas knockdown of SLUG attenuated invasion and prolonged survival in an intracranial mouse model (167).…”

Section: Twist Snail Slug and Zebmentioning

confidence: 99%

Molecular Mechanisms of Glioma Cell Motility

et al. 2017

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Gliomas are the most common intracranial tumors in humans. The most malignant among these tumors is glioblastoma (GBM), with an incidence of 3-5 out of 100,000 persons in Western countries. GBM arises either de novo (primary GBM) or develops from a lower grade glioma (secondary GBM). The prognosis is poor. GBMs are lethal tumors and even optimal surgical resection, followed by chemotherapy and irradiation, results in a median survival of about 12-15 months. One characteristic that is responsible for GBM malignancy, and its worse prognosis, is the highly infiltrative growth of GBM cells into the healthy brain. GBM cell migration and invasion is a very complex process that is regulated by several factors, which include changes in the migrating cell itself as well as the tumor microenvironment. This chapter provides an overview of routes of invasion of glioma cells, the signaling pathways that drive glioma cell motility, and the processes through which glioma cells modulate their surrounding environment.

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SNAI2/Slug promotes growth and invasion in human gliomas

Cited by 134 publications

References 27 publications

Angiopoietin-like protein 1 suppresses SLUG to inhibit cancer cell motility

Angiopoietin-like protein 1 suppresses SLUG to inhibit cancer cell motility

Nuclear phosphorylated Y142 β-catenin accumulates in astrocytomas and glioblastomas and regulates cell invasion

Molecular Mechanisms of Glioma Cell Motility

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