Fra-1 controls motility of bladder cancer cells via transcriptional upregulation of the receptor tyrosine kinase AXL

A. E. Sayan; R. Stanford; R. Vickery; E. Grigorenko; J. Diesch; K. Kulbicki; R. Edwards; R. Pal; P. Greaves; I. Jariel-Encontre; M. Piechaczyk; M. Kriajevska; J. K. Mellon; A. S. Dhillon; E. Tulchinsky

doi:10.1038/onc.2011.336

Fra-1 controls motility of bladder cancer cells via transcriptional upregulation of the receptor tyrosine kinase AXL

A. E. Sayan, R. Stanford, R. Vickery, E. Grigorenko, J. Diesch, K. Kulbicki, R. Edwards, R. Pal, P. Greaves, I. Jariel-Encontre, M. Piechaczyk, M. Kriajevska, J. K. Mellon, A. S. Dhillon, E. Tulchinsky

Research output: Contribution to journal › Article › peer-review

84 Citations (Scopus)

Abstract

Fos-related antigen 1 (Fra-1) is a Fos family member overexpressed in several types of human cancers. Here, we report that Fra-1 is highly expressed in the muscle-invasive form of the carcinoma of the bladder (80%) and to a lesser extent in superficial bladder cancer (42%). We demonstrate that in this type of cancer Fra-1 is regulated via a C-terminal instability signal and C-terminal phosphorylation. We show that manipulation of Fra-1 expression levels in bladder cancer cell lines affects cell morphology, motility and proliferation. The gene coding for AXL tyrosine kinase is directly upregulated by Fra-1 in bladder cancer and in other cell lines. Importantly, our data demonstrate that AXL mediates the effect of Fra-1 on tumour cell motility but not on cell proliferation. We suggest that AXL may represent an attractive therapeutic target in cancers expressing high Fra-1 levels.

Original language	English
Pages (from-to)	1493-1503
Number of pages	11
Journal	Oncogene
Volume	31
Issue number	12
DOIs	https://doi.org/10.1038/onc.2011.336
Publication status	Published - Mar 22 2012
Externally published	Yes

Keywords

bladder cancer
cell motility
Fos-related antigen-1

ASJC Scopus subject areas

Molecular Biology
Genetics
Cancer Research

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1038/onc.2011.336

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Sayan, A. E., Stanford, R., Vickery, R., Grigorenko, E., Diesch, J., Kulbicki, K., Edwards, R., Pal, R., Greaves, P., Jariel-Encontre, I., Piechaczyk, M., Kriajevska, M., Mellon, J. K., Dhillon, A. S., & Tulchinsky, E. (2012). Fra-1 controls motility of bladder cancer cells via transcriptional upregulation of the receptor tyrosine kinase AXL. Oncogene, 31(12), 1493-1503. https://doi.org/10.1038/onc.2011.336

Sayan, AE, Stanford, R, Vickery, R, Grigorenko, E, Diesch, J, Kulbicki, K, Edwards, R, Pal, R, Greaves, P, Jariel-Encontre, I, Piechaczyk, M, Kriajevska, M, Mellon, JK, Dhillon, AS & Tulchinsky, E 2012, 'Fra-1 controls motility of bladder cancer cells via transcriptional upregulation of the receptor tyrosine kinase AXL', Oncogene, vol. 31, no. 12, pp. 1493-1503. https://doi.org/10.1038/onc.2011.336

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abstract = "Fos-related antigen 1 (Fra-1) is a Fos family member overexpressed in several types of human cancers. Here, we report that Fra-1 is highly expressed in the muscle-invasive form of the carcinoma of the bladder (80%) and to a lesser extent in superficial bladder cancer (42%). We demonstrate that in this type of cancer Fra-1 is regulated via a C-terminal instability signal and C-terminal phosphorylation. We show that manipulation of Fra-1 expression levels in bladder cancer cell lines affects cell morphology, motility and proliferation. The gene coding for AXL tyrosine kinase is directly upregulated by Fra-1 in bladder cancer and in other cell lines. Importantly, our data demonstrate that AXL mediates the effect of Fra-1 on tumour cell motility but not on cell proliferation. We suggest that AXL may represent an attractive therapeutic target in cancers expressing high Fra-1 levels.",

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AU - Kulbicki, K.

AU - Edwards, R.

AU - Pal, R.

AU - Greaves, P.

AU - Jariel-Encontre, I.

AU - Piechaczyk, M.

AU - Kriajevska, M.

AU - Mellon, J. K.

AU - Dhillon, A. S.

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Fra-1 controls motility of bladder cancer cells via transcriptional upregulation of the receptor tyrosine kinase AXL

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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