ArticleSmall GTPases2011
FLIM-FRET imaging in vivo reveals 3D-environment spatially regulates RhoGTPase activity during cancer cell invasion.
Article in Small GTPases, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Raman Imaging and Fluorescence Lifetime Imaging Microscopy for Diagnosis of Cancer State and Metabolic Monitoring.Cancers · 2021Review
- Luminescence lifetime imaging of three-dimensional biological objects.Journal of cell science · 2021Article
- A Guide to Fluorescence Lifetime Microscopy and Förster's Resonance Energy Transfer in Neuroscience.Current protocols in neuroscience · 2020Review
- Shedding new light on RhoA signalling as a drug targetSmall GTPases · 2020Article
- Frontiers in Intravital Multiphoton Microscopy of Cancer.Cancer reports (Hoboken, N.J.) · 2020Review
- Article
- Preclinical Advances with Multiphoton Microscopy in Live Imaging of Skin Cancers.The Journal of investigative dermatology · 2017Review
- A simple approach for measuring FRET in fluorescent biosensors using two-photon microscopy.Nature protocols · 2016Article
- Rho-associated kinase signalling and the cancer microenvironment: novel biological implications and therapeutic opportunities.Expert reviews in molecular medicine · 2015Review
- Macrophage contact induces RhoA GTPase signaling to trigger tumor cell intravasation.Oncogene · 2014Article
- Imaging hallmarks of cancer in living mice.Nature reviews. Cancer · 2014Review
- Developments in preclinical cancer imaging: innovating the discovery of therapeutics.Nature reviews. Cancer · 2014Review
- The Rac-FRET mouse reveals tight spatiotemporal control of Rac activity in primary cells and tissues.Cell reports · 2014Article
- Monitoring the dynamics of Src activity in response to anti-invasive dasatinib treatment at a subcellular level using dual intravital imaging.Cell adhesion & migration · 2014Article
- Extracellular signal-regulated kinase regulates RhoA activation and tumor cell plasticity by inhibiting guanine exchange factor H1 activity.Molecular and cellular biology · 2013Article
- Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Many conceptual advances in biology have been achieved by experimental studies using planar two-dimensional cell culture systems. Recent adaptations of molecular techniques to three-dimensional model systems are bridging the gap in our understanding of biological events in vitro and in vivo in the study of disease progression. Recently, in vitro studies using Förster resonance energy transfer (FRET) have shown that the prototypical RhoGTPases Cdc42, Rac and RhoA are temporally and spatially synchronized during cell migration, with initial RhoA activity inducing protrusion prior to activation of Rac. This simultaneous FRET approach illustrates the tight control and dynamic regulation of RhoGTPase activity necessary for coordinated cell migration in vitro. Here, we discuss our recent work using FLIM-FRET analysis in a three-dimensional setting to reveal another layer of regulation in which RhoA activity is governed by the extracellular microenvironment. We demonstrate that RhoA is spatially regulated into discrete fractions of activity at the leading edge and rear of cells during invasion in vivo or within three-dimensional matrices. Significantly, this spatial regulation of RhoA was absent in two-dimensional in vitro settings. This distinct sub-cellular regulation of RhoA at the poles of invading cells in three-dimensions sets a precedent that other RhoGTPases or signaling proteins may also be differentially regulated in a con-text-dependent manner during key biological processes such as invasion.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.