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FHOD1, a Formin Upr...
FHOD1, a Formin Upregulated in Epithelial-Mesenchymal Transition, Participates in Cancer Cell Migration and Invasion
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Gardberg, M. (author)
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Kaipio, K. (author)
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Lehtinen, L. (author)
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Mikkonen, P. (author)
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Heuser, V. D. (author)
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Talvinen, K. (author)
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Iljin, K. (author)
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- Kampf, Caroline (author)
- Uppsala universitet,Molekylär och morfologisk patologi
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- Uhlén, Mathias (author)
- KTH,Proteomik och nanobioteknologi,Science for Life Laboratory, SciLifeLab
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Grénman, R. (author)
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Koivisto, M. (author)
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Carpén, O. (author)
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(creator_code:org_t)
- 2013-09-26
- 2013
- English.
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In: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:9, s. e74923-
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https://uu.diva-port... (primary) (Raw object)
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Abstract
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- Cancer cells can obtain their ability to invade and metastasise by undergoing epithelial-to-mesenchymal transition (EMT). Exploiting this mechanism of cellular plasticity, malignant cells can remodel their actin cytoskeleton and down-regulate proteins needed for cell-cell contacts. The mechanisms of cytoskeletal reorganisation resulting in mesenchymal morphology and increased invasive potential are poorly understood. Actin nucleating formins have been implicated as key players in EMT. Here, we analysed which formins are altered in squamous cell carcinoma related EMT. FHOD1, a poorly studied formin, appeared to be markedly upregulated upon EMT. In human tissues FHOD1 was primarily expressed in mesenchymal cells, with little expression in epithelia. However, specimens from oral squamous cell cancers demonstrated consistent FHOD1 upregulation in mesenchymally transformed cells at the invasive edge. This upregulation was confirmed in an oral squamous carcinoma model, where FHOD1 expression was markedly increased upon EMT in a PI3K signalling dependent manner. In the EMT cells FHOD1 contributed to the spindle-shaped morphology and mesenchymal F-actin organization. Furthermore, functional assays demonstrated that FHOD1 contributes to cell migration and invasion. Finally, FHOD1 depletion reduced the ability of EMT cancer cells to form invadopodia and to degrade extracellular matrix. Our results indicate that FHOD1 participates in cytoskeletal changes in EMT. In addition, we show that FHOD1 upregulation occurs during cancer cell EMT in vivo, which indicates that FHOD1 may contribute to tumour progression.
Subject headings
- NATURVETENSKAP -- Biologi (hsv//swe)
- NATURAL SCIENCES -- Biological Sciences (hsv//eng)
Keyword
- Invadopodia Formation
- Protein Fhod1
- Carcinoma-Cells
- Domain
- Rock
- Tissues
- Fmnl2
- Rac
Publication and Content Type
- ref (subject category)
- art (subject category)
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- By the author/editor
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Gardberg, M.
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Kaipio, K.
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Lehtinen, L.
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Mikkonen, P.
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Heuser, V. D.
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Talvinen, K.
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show more...
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Iljin, K.
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Kampf, Caroline
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Uhlén, Mathias
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Grénman, R.
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Koivisto, M.
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Carpén, O.
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show less...
- About the subject
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- NATURAL SCIENCES
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NATURAL SCIENCES
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and Biological Scien ...
- Articles in the publication
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PLOS ONE
- By the university
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Royal Institute of Technology
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Uppsala University