Tumor-suppressive activity of the growth arrest-specific gene GAS1 in human tumor cell lines

Evdokiou, Andreas; Cowled, Prue

doi:10.1002/(sici)1097-0215(19980209)75:4<568::aid-ijc13>3.0.co;2-5

Cited by 49 publications

(24 citation statements)

References 15 publications

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“…Reduced affinity for Gas1 would increase the availability of SHH and lead to excessive SHH signaling, resulting in dysregulated growth. Although GAS1 can suppress tumor cell growth and is deleted in some myeloid tumors (37,38), it has not been directly implicated in basal cell carcinoma, a condition frequently associated with excessive SHH signaling (25,(39)(40)(41). It is not yet known whether Gas1 plays a role in Shh-related tumorigenesis.…”

Section: Discussionmentioning

confidence: 99%

Evidence that the WNT-inducible growth arrest-specific gene 1 encodes an antagonist of sonic hedgehog signaling in the somite

Lee

Buttitta

Fan

2001

Proc. Natl. Acad. Sci. U.S.A.

158

130

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The dorsal-ventral polarity of the somite is controlled by antagonistic signals from the dorsal neural tube͞surface ectoderm, mediated by WNTs, and from the ventral notochord, mediated by sonic hedgehog (SHH). Each factor can act over a distance greater than a somite diameter in vitro, suggesting they must limit each other's actions within their own patterning domains in vivo. We show here that the growth-arrest specific gene 1 (Gas1), which is expressed in the dorsal somite, is induced by WNTs and encodes a protein that can bind to SHH. Furthermore, ectopic expression of Gas1 in presomitic cells attenuates the response of these cells to SHH in vitro. Taken together, these data suggest that GAS1 functions to reduce the availability of active SHH within the dorsal somite.

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Section: Discussionmentioning

confidence: 99%

Evidence that the WNT-inducible growth arrest-specific gene 1 encodes an antagonist of sonic hedgehog signaling in the somite

Lee

Buttitta

Fan

2001

Proc. Natl. Acad. Sci. U.S.A.

158

130

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“…18 Ectopic expression of Gas1 inhibits fibroblast and tumor cell proliferation in a p53-dependent way. [19][20][21] However, Gas1 mechanism of action is largely unknown and its activities may vary in different cell systems 22,23 and in the embryo. 24,25 In this article we show that expression of Gas1 in endothelial cells does not significantly inhibit cell growth but strongly protects the cells from apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Gas1 is induced by VE-cadherin and vascular endothelial growth factor and inhibits endothelial cell apoptosis

Spagnuolo

Corada

Orsenigo

et al. 2004

Blood

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“…The cDNA sequences of these Gas genes show no similarity. Their activities have been found to range from the control of nerve cell differentiation to the regulation of microfilament organization, apoptosis, cell proliferation, and cell cycling (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). We previously reported the use of retroviral based gene search vectors to identify two murine chromosomal loci (354 -6 and 354 -7) whose expression in fibroblasts is activated during growth arrest (13).…”

mentioning

confidence: 99%

Isolation and Properties of Gas8, a Growth Arrest-specific Gene Regulated during Male Gametogenesis to Produce a Protein Associated with the Sperm Motility Apparatus

Yeh¹,

Chen²,

Chang³

et al. 2002

Journal of Biological Chemistry

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Growth arrest-specific (Gas) genes are expressed during serum starvation or contact inhibition of cells grown in culture. Here we report the isolation and characterization of Gas8, a novel gene identified on the basis of its growth arrest-specific expression in murine fibroblasts. We show that production of Gas8 mRNA and protein occurs in adult mice predominantly in the testes, where expression is regulated during postmeiotic development of male gametocytes. Whereas a low level of Gas8 mRNA was detected by Northern blotting in testes of murine male neonates and young adolescents, Gas8 mRNA increased rapidly postmeiotically. In adult males, both Gas8 mRNA and protein reached steady state levels in testes that were 10-fold higher than in other tissues. Immunohistochemical analyses showed that Gas8 protein accumulates in gametocytes as they approach the lumen of seminiferous tubules and is localized to the cytoplasm of round spermatids, the tails of elongating spermatids, and mature spermatid tail bundles protruding into the lumen; in epididymal spermatozoa Gas8 protein was present in the flagella. However, premeiotic murine gametocytes lacked detectable Gas8 protein, as did seminiferous tubules in biopsy specimens from seven human males having cytological evidence of nonobstructive azoospermia secondary to Sertoli cell-only syndrome. Our findings, which associate Gas8 production developmentally with the later stages of spermatogenesis and spatially with the sperm motility apparatus, collectively suggest that this growth arrest-specific gene product may have a role in sperm motility. This postulated role for Gas8 is supported by our observation that highly localized production of Gas8 protein occurs also in the cilia of epithelial cells lining pulmonary bronchi and fallopian tubes and by the flagellar association of a Trypanosoma brucei ortholog of Gas8.

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Tumor-suppressive activity of the growth arrest-specific gene GAS1 in human tumor cell lines

Cited by 49 publications

References 15 publications

Evidence that the WNT-inducible growth arrest-specific gene 1 encodes an antagonist of sonic hedgehog signaling in the somite

Evidence that the WNT-inducible growth arrest-specific gene 1 encodes an antagonist of sonic hedgehog signaling in the somite

Gas1 is induced by VE-cadherin and vascular endothelial growth factor and inhibits endothelial cell apoptosis

Isolation and Properties of Gas8, a Growth Arrest-specific Gene Regulated during Male Gametogenesis to Produce a Protein Associated with the Sperm Motility Apparatus

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