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Restoration of contact inhibition in human glioblastoma cell lines after MIF knockdown.

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Restoration of contact inhibition in human glioblastoma cell lines after MIF knockdown. / Schrader, Jörg; Deuster, Oliver; Rinn, Birgit; Schulz, Martina; Kautz, Andreas; Dodel, Richard; Meyer, Bernhard; Al-Abed, Yousef; Balakrishnan, Karthikeyan; Reese, Jens P; Bacher, Michael.

In: BMC CANCER, Vol. 9, 2009, p. 464.

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

Harvard

Schrader, J, Deuster, O, Rinn, B, Schulz, M, Kautz, A, Dodel, R, Meyer, B, Al-Abed, Y, Balakrishnan, K, Reese, JP & Bacher, M 2009, 'Restoration of contact inhibition in human glioblastoma cell lines after MIF knockdown.', BMC CANCER, vol. 9, pp. 464. https://doi.org/10.1186/1471-2407-9-464

APA

Schrader, J., Deuster, O., Rinn, B., Schulz, M., Kautz, A., Dodel, R., Meyer, B., Al-Abed, Y., Balakrishnan, K., Reese, J. P., & Bacher, M. (2009). Restoration of contact inhibition in human glioblastoma cell lines after MIF knockdown. BMC CANCER, 9, 464. https://doi.org/10.1186/1471-2407-9-464

Vancouver

Schrader J, Deuster O, Rinn B, Schulz M, Kautz A, Dodel R et al. Restoration of contact inhibition in human glioblastoma cell lines after MIF knockdown. BMC CANCER. 2009;9:464. https://doi.org/10.1186/1471-2407-9-464

Bibtex

@article{de7463c1f4b040218438e6cb31dbb5a6,
title = "Restoration of contact inhibition in human glioblastoma cell lines after MIF knockdown.",
abstract = "BACKGROUND: Studies of the role of the cytokine macrophage-migration-inhibitory-factor (MIF) in malignant tumors have revealed its stimulating influence on cell-cycle progression, angiogenesis and anti-apoptosis. RESULTS: Here we show that in vitro targeting MIF in cultures of human malignant glioblastoma cells by either antisense plasmid introduction or anti-MIF antibody treatment reduced the growth rates of tumor cells. Of note is the marked decrease of proliferation under confluent and over-confluent conditions, implying a role of MIF in overcoming contact inhibition. Several proteins involved in contact inhibition including p27, p21, p53 and CEBPalpha are upregulated in the MIF antisense clones indicating a restoration of contact inhibition in the tumor cells. Correspondingly, we observed a marked increase in MIF mRNA and protein content under higher cell densities in LN18 cells. Furthermore, we showed the relevance of the enzymatic active site of MIF for the proliferation of glioblastoma cells by using the MIF-tautomerase inhibitor ISO-1. CONCLUSION: Our study adds another puzzle stone to the role of MIF in tumor growth and progression by showing the importance of MIF for overcoming contact inhibition.",
author = "J{\"o}rg Schrader and Oliver Deuster and Birgit Rinn and Martina Schulz and Andreas Kautz and Richard Dodel and Bernhard Meyer and Yousef Al-Abed and Karthikeyan Balakrishnan and Reese, {Jens P} and Michael Bacher",
year = "2009",
doi = "10.1186/1471-2407-9-464",
language = "Deutsch",
volume = "9",
pages = "464",
journal = "BMC CANCER",
issn = "1471-2407",
publisher = "BioMed Central Ltd.",

}

RIS

TY - JOUR

T1 - Restoration of contact inhibition in human glioblastoma cell lines after MIF knockdown.

AU - Schrader, Jörg

AU - Deuster, Oliver

AU - Rinn, Birgit

AU - Schulz, Martina

AU - Kautz, Andreas

AU - Dodel, Richard

AU - Meyer, Bernhard

AU - Al-Abed, Yousef

AU - Balakrishnan, Karthikeyan

AU - Reese, Jens P

AU - Bacher, Michael

PY - 2009

Y1 - 2009

N2 - BACKGROUND: Studies of the role of the cytokine macrophage-migration-inhibitory-factor (MIF) in malignant tumors have revealed its stimulating influence on cell-cycle progression, angiogenesis and anti-apoptosis. RESULTS: Here we show that in vitro targeting MIF in cultures of human malignant glioblastoma cells by either antisense plasmid introduction or anti-MIF antibody treatment reduced the growth rates of tumor cells. Of note is the marked decrease of proliferation under confluent and over-confluent conditions, implying a role of MIF in overcoming contact inhibition. Several proteins involved in contact inhibition including p27, p21, p53 and CEBPalpha are upregulated in the MIF antisense clones indicating a restoration of contact inhibition in the tumor cells. Correspondingly, we observed a marked increase in MIF mRNA and protein content under higher cell densities in LN18 cells. Furthermore, we showed the relevance of the enzymatic active site of MIF for the proliferation of glioblastoma cells by using the MIF-tautomerase inhibitor ISO-1. CONCLUSION: Our study adds another puzzle stone to the role of MIF in tumor growth and progression by showing the importance of MIF for overcoming contact inhibition.

AB - BACKGROUND: Studies of the role of the cytokine macrophage-migration-inhibitory-factor (MIF) in malignant tumors have revealed its stimulating influence on cell-cycle progression, angiogenesis and anti-apoptosis. RESULTS: Here we show that in vitro targeting MIF in cultures of human malignant glioblastoma cells by either antisense plasmid introduction or anti-MIF antibody treatment reduced the growth rates of tumor cells. Of note is the marked decrease of proliferation under confluent and over-confluent conditions, implying a role of MIF in overcoming contact inhibition. Several proteins involved in contact inhibition including p27, p21, p53 and CEBPalpha are upregulated in the MIF antisense clones indicating a restoration of contact inhibition in the tumor cells. Correspondingly, we observed a marked increase in MIF mRNA and protein content under higher cell densities in LN18 cells. Furthermore, we showed the relevance of the enzymatic active site of MIF for the proliferation of glioblastoma cells by using the MIF-tautomerase inhibitor ISO-1. CONCLUSION: Our study adds another puzzle stone to the role of MIF in tumor growth and progression by showing the importance of MIF for overcoming contact inhibition.

U2 - 10.1186/1471-2407-9-464

DO - 10.1186/1471-2407-9-464

M3 - SCORING: Zeitschriftenaufsatz

VL - 9

SP - 464

JO - BMC CANCER

JF - BMC CANCER

SN - 1471-2407

ER -