Targeting filamin B induces tumor growth and metastasis via enhanced activity of matrix metalloproteinase-9 and secretion of VEGF-A: Role of filamin in tumor growth.

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Bandaru, SashidarGothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology,University of Gothenburg, Sweden (author)

Targeting filamin B induces tumor growth and metastasis via enhanced activity of matrix metalloproteinase-9 and secretion of VEGF-A : Role of filamin in tumor growth.

Article/chapterEnglish2014

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2014-09-22
Springer Science and Business Media LLC,2014

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LIBRIS-ID:oai:gup.ub.gu.se/203336
https://gup.ub.gu.se/publication/203336URI
https://doi.org/10.1038/oncsis.2014.33DOI
https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-114452URI
http://kipublications.ki.se/Default.aspx?queryparsed=id:130535133URI

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Language:English

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Subject category:art swepub-publicationtype

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Funding Agencies|Swedish Society of Medicine; Magnus Bergvalls Foundation; Jubileumfonden; Sahlgrenska University Hospital; Royal Society of Arts and Sciences in Goteborg; Assar Gabrielssons Foundation; Swedish Heart and Lung Foundation; Swedish Research Council; Swedish Cancer Foundation
Filamins regulate cell locomotion and associate with diverse signaling molecules. We have recently found that targeting filamin A (FLNA) reduces RAS-induced lung adenocarcinomas. In this study, we explored the role of another major filamin isoform, filamin B (FLNB), in tumor development. In contrast to FLNA, we report that targeting FLNB enhances RAS-induced tumor growth and metastasis which is associated with higher matrix metallopeptidase-9 (MMP-9) and extracellular signal-regulated kinase (ERK) activity. Flnb deficiency in mouse embryonic fibroblasts results in increased proteolytic activity of MMP-9 and cell invasion mediated by the RAS/ERK pathway. Similarly, silencing FLNB in multiple human cancer cells increases the proteolytic activity of MMP-9 and tumor cell invasion. Furthermore, we observed that Flnb-deficient RAS-induced tumors display more capillary structures that is correlated with increased vascular endothelial growth factor-A (VEGF-A) secretion. Inhibition of ERK activation blocks phorbol myristate acetate-induced MMP-9 activity and VEGF-A secretion in vitro. In addition, silencing FLNB in human ovarian cancer cells increases secretion of VEGF-A that induces endothelial cells to form more vascular structures in vitro. We conclude that FLNB suppresses tumor growth and metastasis by regulating the activity of MMP-9 and secretion of VEGF-A which is mediated by the RAS/ERK pathway.

Subject headings and genre

MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Medicinsk genetik hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Medical Genetics hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Medicinska och farmaceutiska grundvetenskaper Cell- och molekylärbiologi hsv//swe
MEDICAL AND HEALTH SCIENCES Basic Medicine Cell and Molecular Biology hsv//eng
MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine hsv//eng
cancer
metastasis growth
mouse
zebrafish

Added entries (persons, corporate bodies, meetings, titles ...)

Zhou, Xianghua,1973Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology,University of Gothenburg, Sweden(Swepub:gu)xzhoxi (author)
Rouhi, PegahKarolinska Institute, Sweden (author)
Zhang, YanKarolinska Institutet (author)
Bergö, Martin,1970Gothenburg University,Göteborgs universitet,Sahlgrenska Cancer Center,University of Gothenburg, Sweden(Swepub:gu)xbmarl (author)
Cao, YihaiKarolinska Institutet,Linköpings universitet,Avdelningen för kardiovaskulär medicin,Hälsouniversitetet,Karolinska Institute, Sweden(Swepub:liu)yihca64 (author)
Akyürek, Levent,1966Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi,Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology,University of Gothenburg, Sweden; Sahlgrens University Hospital, Sweden(Swepub:gu)xakyle (author)
Göteborgs universitetInstitutionen för biomedicin, avdelningen för medicinsk kemi och cellbiologi (creator_code:org_t)

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