The interplay between the proteolytic, invasive, and adhesive domains of invadopodia and their roles in cancer invasion

Revach, Or‐Yam; Geiger, Benjamin

doi:10.4161/cam.27842

Cited by 59 publications

(56 citation statements)

References 146 publications

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“…As actin filaments elongate, they can push against any physical obstacle they encounter. Such a pushing mechanism can drive the leading edge of the cell forward during migration (Keren et al, 2008;Mogilner and Oster, 1996;Pollard et al, 2001), and extend thin protrusions to probe the surrounding ECM by using filopodia (Mattila and Lappalainen, 2008) or invade it with invadopodia (Buccione et al, 2004;Revach and Geiger, 2014). It is important to note, however, that cellular pushing does not necessarily take place through cytoskeletal polymerization, as in the cases of bleb (Fackler and Grosse, 2008) and lobopodium formation (Petrie et al, 2014), which are driven by the hydrostatic pressure in the cell.…”

Section: Introduction -Cellular Mechanosensitivity As An Emerging Parmentioning

confidence: 99%

The inner workings of stress fibers − from contractile machinery to focal adhesions and back

Livne

Geiger

2016

Journal of Cell Science

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167

153

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Ventral stress fibers and focal adhesions are physically coupled structures that play key roles in cellular mechanics and force sensing. The tight functional interdependence between the two is manifested not only by their apparent proximity but also by the fact that ventral stress fibers and focal adhesions are simultaneously diminished upon actomyosin relaxation, and grow when subjected to external stretching. However, whereas the apparent co-regulation of the two structures is well-documented, the underlying mechanisms remains poorly understood. In this Commentary, we discuss some of the fundamental, yet still open questions regarding ventral stress fiber structure, its force-dependent assembly, as well as its capacity to generate force. We also challenge the common approach -i.e. ventral stress fibers are variants of the well-studied striated or smooth muscle machinery -by presenting and critically discussing alternative venues. By highlighting some of the less-explored aspects of the interplay between stress fibers and focal adhesions, we hope that this Commentary will encourage further investigation in this field.

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Section: Introduction -Cellular Mechanosensitivity As An Emerging Parmentioning

confidence: 99%

The inner workings of stress fibers − from contractile machinery to focal adhesions and back

Livne

Geiger

2016

Journal of Cell Science

Self Cite

167

153

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“…82,145,149,154 It is unclear why both growth factor signaling and adhesion signaling are needed for invasion-the connection between adhesion and growth factor signaling in invadopod formation is an active area of investigation. [155][156][157][158][159] MicroRNAs THAT REGULATE HNSCC INVASION MicroRNAs (miRNAs) are a class of gene-expression regulators that often have altered expression in various human cancers, including HNSCC. [160][161][162][163][164][165] The MiRNAs have emerged as having key roles in diverse cellular processes, including cancer cell proliferation, migration, invasion, and metastasis.…”

mentioning

confidence: 99%

Mechanisms of Invasion in Head and Neck Cancer

Jimenez¹,

Jayakar²,

Ow³

et al. 2015

Archives of Pathology &Amp; Laboratory Medicine

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Context.-The highly invasive properties demonstrated by head and neck squamous cell carcinoma (HNSCC) are often associated with locoregional recurrence and lymph node metastasis in patients and is a key factor leading to an expected 5-year survival rate of approximately 50% for patients with advanced disease. It is important to understand the features and mediators of HNSCC invasion so that new treatment approaches can be developed.Objectives.-To provide an overview of the characteristics, mediators, and mechanisms of HNSCC invasion.Data Sources.-A literature review of peer-reviewed articles in PubMed on HNSCC invasion.Conclusions.-Histologic features of HNSCC tumors can help predict prognosis and influence clinical treatment decisions. Cell surface receptors, signaling pathways, proteases, invadopodia function, epithelial-mesenchymal transition, microRNAs, and tumor microenvironment are all involved in the regulation of the invasive behavior of HNSCC cells. Identifying effective HNSCC invasion inhibitors has the potential to improve outcomes for patients by reducing the rate of spread and increasing responsiveness to chemoradiation.

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“…Invadopodia are large assemblies that mediate cell invasion Paz et al, 2014;Revach and Geiger, 2014). We found that talin2 colocalized with invadopodia to a considerable extent (Fig.…”

Section: Discussionmentioning

confidence: 83%

Talin2-mediated traction force drives matrix degradation and cell invasion

Jafari

et al. 2016

Journal of Cell Science

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Talin binds to β-integrin tails to activate integrins, regulating cell migration, invasion and metastasis. There are two talin genes, TLN1 and TLN2, encoding talin1 and talin2, respectively. Talin1 regulates focal adhesion dynamics, cell migration and invasion, whereas the biological function of talin2 is not clear and, indeed, talin2 has been presumed to function redundantly with talin1. Here, we show that talin2 has a much stronger binding to β-integrin tails than talin1. Replacement of talin2 Ser339 with Cys significantly decreased its binding to β1-integrin tails to a level comparable to that of talin1. Talin2 localizes at invadopodia and is indispensable for the generation of traction force and invadopodium-mediated matrix degradation. Ablation of talin2 suppressed traction force generation and invadopodia formation, which were restored by re-expressing talin2 but not talin1. Furthermore, re-expression of wild-type talin2 (but not talin2 S339C ) in talin2-depleted cells rescued development of traction force and invadopodia. These results suggest that a strong interaction of talin2 with integrins is required to generate traction, which in turn drives invadopodium-mediated matrix degradation, which is key to cancer cell invasion.

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The interplay between the proteolytic, invasive, and adhesive domains of invadopodia and their roles in cancer invasion

Cited by 59 publications

References 146 publications

The inner workings of stress fibers − from contractile machinery to focal adhesions and back

The inner workings of stress fibers − from contractile machinery to focal adhesions and back

Mechanisms of Invasion in Head and Neck Cancer

Talin2-mediated traction force drives matrix degradation and cell invasion

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