Myosin isoform expressed in metastatic prostate cancer stimulates cell invasion

Abstract During metastasis, tumor cells migrate out of their original tissue to invade other organs. Secretion of exosomes and metalloproteases is essential for extracellular matrix remodeling, enabling migration through tissue barriers. Metastatic prostate cancer is differentiated by expression of...

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Autores principales:	Ivan V. Maly, Tera M. Domaradzki, Victoria A. Gosy, Wilma A. Hofmann
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8b23fe178b9a4605973128c7b29c8250
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spelling	oai:doaj.org-article:8b23fe178b9a4605973128c7b29c82502021-12-02T16:06:23ZMyosin isoform expressed in metastatic prostate cancer stimulates cell invasion10.1038/s41598-017-09158-52045-2322https://doaj.org/article/8b23fe178b9a4605973128c7b29c82502017-08-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-09158-5https://doaj.org/toc/2045-2322Abstract During metastasis, tumor cells migrate out of their original tissue to invade other organs. Secretion of exosomes and metalloproteases is essential for extracellular matrix remodeling, enabling migration through tissue barriers. Metastatic prostate cancer is differentiated by expression of the rare isoform A of the molecular motor myosin IC, however the function of this isoform remained unknown. Here we show that it contributes causatively to the invasive motility of prostate cancer cells. We found that the isoform associates with metalloprotease-containing exosomes and stimulates their secretion. While the data show that myosin IC is involved in prostate cancer cell migration, migration outside extracellular matrix in vitro proves little affected specifically by isoform A. Nevertheless, this isoform stimulates invasion through extracellular matrix, pointing to a critical role in secretion. Both the secretion and invasion depend on the integrity of the motor and lipid-binding domains of the protein. Our results demonstrate how myosin IC isoform A is likely to function in metastasis, driving secretion of exosomes that enable invasion of prostate cancer cells across extracellular matrix barriers. The new data identify a molecule suitable for a mechanistically grounded development into a marker and target for prognosis, detection, and treatment of invasive prostate cancer.Ivan V. MalyTera M. DomaradzkiVictoria A. GosyWilma A. HofmannNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-10 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Ivan V. Maly Tera M. Domaradzki Victoria A. Gosy Wilma A. Hofmann Myosin isoform expressed in metastatic prostate cancer stimulates cell invasion
description	Abstract During metastasis, tumor cells migrate out of their original tissue to invade other organs. Secretion of exosomes and metalloproteases is essential for extracellular matrix remodeling, enabling migration through tissue barriers. Metastatic prostate cancer is differentiated by expression of the rare isoform A of the molecular motor myosin IC, however the function of this isoform remained unknown. Here we show that it contributes causatively to the invasive motility of prostate cancer cells. We found that the isoform associates with metalloprotease-containing exosomes and stimulates their secretion. While the data show that myosin IC is involved in prostate cancer cell migration, migration outside extracellular matrix in vitro proves little affected specifically by isoform A. Nevertheless, this isoform stimulates invasion through extracellular matrix, pointing to a critical role in secretion. Both the secretion and invasion depend on the integrity of the motor and lipid-binding domains of the protein. Our results demonstrate how myosin IC isoform A is likely to function in metastasis, driving secretion of exosomes that enable invasion of prostate cancer cells across extracellular matrix barriers. The new data identify a molecule suitable for a mechanistically grounded development into a marker and target for prognosis, detection, and treatment of invasive prostate cancer.
format	article
author	Ivan V. Maly Tera M. Domaradzki Victoria A. Gosy Wilma A. Hofmann
author_facet	Ivan V. Maly Tera M. Domaradzki Victoria A. Gosy Wilma A. Hofmann
author_sort	Ivan V. Maly
title	Myosin isoform expressed in metastatic prostate cancer stimulates cell invasion
title_short	Myosin isoform expressed in metastatic prostate cancer stimulates cell invasion
title_full	Myosin isoform expressed in metastatic prostate cancer stimulates cell invasion
title_fullStr	Myosin isoform expressed in metastatic prostate cancer stimulates cell invasion
title_full_unstemmed	Myosin isoform expressed in metastatic prostate cancer stimulates cell invasion
title_sort	myosin isoform expressed in metastatic prostate cancer stimulates cell invasion
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/8b23fe178b9a4605973128c7b29c8250
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Myosin isoform expressed in metastatic prostate cancer stimulates cell invasion

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