Cancer predisposition in mice deficient for the metastasis-associated Mts1(S100A4) gene

Research output: Contribution to journal › Journal article › Research › peer-review

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Cancer predisposition in mice deficient for the metastasis-associated Mts1(S100A4) gene. / Naaman, Christina E.L.; Grum-Schwensen, Birgitte; Mansouri, Ahmed; Grigorian, Mariam; Santoni-Rugiu, Eric; Hansen, Thomas; Kriajevska, Marina; Schafer, Beat W.; Heizmann, Claus W.; Lukanidin, Eugene; Ambartsumian, Noona.

In: Oncogene, Vol. 23, No. 20, 29.04.2004, p. 3670-3680.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Naaman, CEL, Grum-Schwensen, B, Mansouri, A, Grigorian, M, Santoni-Rugiu, E, Hansen, T, Kriajevska, M, Schafer, BW, Heizmann, CW, Lukanidin, E & Ambartsumian, N 2004, 'Cancer predisposition in mice deficient for the metastasis-associated Mts1(S100A4) gene', Oncogene, vol. 23, no. 20, pp. 3670-3680. https://doi.org/10.1038/sj.onc.1207420

APA

Naaman, C. E. L., Grum-Schwensen, B., Mansouri, A., Grigorian, M., Santoni-Rugiu, E., Hansen, T., Kriajevska, M., Schafer, B. W., Heizmann, C. W., Lukanidin, E., & Ambartsumian, N. (2004). Cancer predisposition in mice deficient for the metastasis-associated Mts1(S100A4) gene. Oncogene, 23(20), 3670-3680. https://doi.org/10.1038/sj.onc.1207420

Vancouver

Naaman CEL, Grum-Schwensen B, Mansouri A, Grigorian M, Santoni-Rugiu E, Hansen T et al. Cancer predisposition in mice deficient for the metastasis-associated Mts1(S100A4) gene. Oncogene. 2004 Apr 29;23(20):3670-3680. https://doi.org/10.1038/sj.onc.1207420

Author

Naaman, Christina E.L. ; Grum-Schwensen, Birgitte ; Mansouri, Ahmed ; Grigorian, Mariam ; Santoni-Rugiu, Eric ; Hansen, Thomas ; Kriajevska, Marina ; Schafer, Beat W. ; Heizmann, Claus W. ; Lukanidin, Eugene ; Ambartsumian, Noona. / Cancer predisposition in mice deficient for the metastasis-associated Mts1(S100A4) gene. In: Oncogene. 2004 ; Vol. 23, No. 20. pp. 3670-3680.

Bibtex

@article{e633851dc50d4d58916237d260332f27,
title = "Cancer predisposition in mice deficient for the metastasis-associated Mts1(S100A4) gene",
abstract = "Metastasis-promoting Mts1(S100A4) protein belongs to the S100 family of Ca2+-binding proteins. A mouse strain with a germ-line inactivation of the S100A4 gene was generated. The mice were viable and did not display developmental abnormalities in the postnatal period. However, an abnormal sex ratio was observed in the litters with the S100A4-/- genotype, raising the possibility of a certain level of embryonic lethality in this strain. In all, 10% of 10-14-month-old S100A4-null animals developed tumors. This is a characteristic feature of mouse strains with inactivated tumor suppressor genes. Spontaneous tumors of S100A4-/- mice were p53 positive. Recently, we have shown that S100A4 interacts with p53 tumor suppressor protein and induces apoptosis. We proposed that impairment of this interaction could affect the apoptosis-promoting function of p53 that is involved in its tumor suppressor activity. The frequency of apoptosis in the spleen of S100A4-/- animals after whole-body γ-irradiation was reduced compared to the wild-type animals. The same was true for the transcriptional activation of the p53 target genes - waf/p21/cip1 and bax. Taken together, these observations indicate that spontaneous tumors in S100A4-/- mice are a result of functional destabilization of p53 tumor suppressor gene.",
keywords = "Animal models, Mts1(S100A4), p53, Tumor development, Tumor suppressor activity",
author = "Naaman, {Christina E.L.} and Birgitte Grum-Schwensen and Ahmed Mansouri and Mariam Grigorian and Eric Santoni-Rugiu and Thomas Hansen and Marina Kriajevska and Schafer, {Beat W.} and Heizmann, {Claus W.} and Eugene Lukanidin and Noona Ambartsumian",
year = "2004",
month = apr,
day = "29",
doi = "10.1038/sj.onc.1207420",
language = "English",
volume = "23",
pages = "3670--3680",
journal = "Oncogene",
issn = "0950-9232",
publisher = "nature publishing group",
number = "20",

}

RIS

TY - JOUR

T1 - Cancer predisposition in mice deficient for the metastasis-associated Mts1(S100A4) gene

AU - Naaman, Christina E.L.

AU - Grum-Schwensen, Birgitte

AU - Mansouri, Ahmed

AU - Grigorian, Mariam

AU - Santoni-Rugiu, Eric

AU - Hansen, Thomas

AU - Kriajevska, Marina

AU - Schafer, Beat W.

AU - Heizmann, Claus W.

AU - Lukanidin, Eugene

AU - Ambartsumian, Noona

PY - 2004/4/29

Y1 - 2004/4/29

N2 - Metastasis-promoting Mts1(S100A4) protein belongs to the S100 family of Ca2+-binding proteins. A mouse strain with a germ-line inactivation of the S100A4 gene was generated. The mice were viable and did not display developmental abnormalities in the postnatal period. However, an abnormal sex ratio was observed in the litters with the S100A4-/- genotype, raising the possibility of a certain level of embryonic lethality in this strain. In all, 10% of 10-14-month-old S100A4-null animals developed tumors. This is a characteristic feature of mouse strains with inactivated tumor suppressor genes. Spontaneous tumors of S100A4-/- mice were p53 positive. Recently, we have shown that S100A4 interacts with p53 tumor suppressor protein and induces apoptosis. We proposed that impairment of this interaction could affect the apoptosis-promoting function of p53 that is involved in its tumor suppressor activity. The frequency of apoptosis in the spleen of S100A4-/- animals after whole-body γ-irradiation was reduced compared to the wild-type animals. The same was true for the transcriptional activation of the p53 target genes - waf/p21/cip1 and bax. Taken together, these observations indicate that spontaneous tumors in S100A4-/- mice are a result of functional destabilization of p53 tumor suppressor gene.

AB - Metastasis-promoting Mts1(S100A4) protein belongs to the S100 family of Ca2+-binding proteins. A mouse strain with a germ-line inactivation of the S100A4 gene was generated. The mice were viable and did not display developmental abnormalities in the postnatal period. However, an abnormal sex ratio was observed in the litters with the S100A4-/- genotype, raising the possibility of a certain level of embryonic lethality in this strain. In all, 10% of 10-14-month-old S100A4-null animals developed tumors. This is a characteristic feature of mouse strains with inactivated tumor suppressor genes. Spontaneous tumors of S100A4-/- mice were p53 positive. Recently, we have shown that S100A4 interacts with p53 tumor suppressor protein and induces apoptosis. We proposed that impairment of this interaction could affect the apoptosis-promoting function of p53 that is involved in its tumor suppressor activity. The frequency of apoptosis in the spleen of S100A4-/- animals after whole-body γ-irradiation was reduced compared to the wild-type animals. The same was true for the transcriptional activation of the p53 target genes - waf/p21/cip1 and bax. Taken together, these observations indicate that spontaneous tumors in S100A4-/- mice are a result of functional destabilization of p53 tumor suppressor gene.

KW - Animal models

KW - Mts1(S100A4)

KW - p53

KW - Tumor development

KW - Tumor suppressor activity

UR - http://www.scopus.com/inward/record.url?scp=2442696687&partnerID=8YFLogxK

U2 - 10.1038/sj.onc.1207420

DO - 10.1038/sj.onc.1207420

M3 - Journal article

C2 - 15116098

AN - SCOPUS:2442696687

VL - 23

SP - 3670

EP - 3680

JO - Oncogene

JF - Oncogene

SN - 0950-9232

IS - 20

ER -

ID: 257666852