ArticleBiochemical and biophysical research communications2018
Cdc42-dependent modulation of rigidity sensing and cell spreading in tumor repopulating cells.
Article in Biochemical and biophysical research communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Cytoskeletal Prestress Regulates RIG-I-Mediated Innate Immunity.Biophysica · 2025Article
- Hybrid AI models allow label-free identification and classification of pancreatic tumor repopulating cell population.Biochemical and biophysical research communications · 2023Article
- Understanding How Cells Probe the World: A Preliminary Step towards Modeling Cell Behavior?International journal of molecular sciences · 2023Article
- Synthetic Retinoid Kills Drug-Resistant Cancer Stem Cells via Inducing RARγ-Translocation-Mediated Tension Reduction and Chromatin Decondensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Cytoskeletal prestress: The cellular hallmark in mechanobiology and mechanomedicine.Cytoskeleton (Hoboken, N.J.) · 2021Review
- COL2A1 Is a Novel Biomarker of Melanoma Tumor Repopulating Cells.Biomedicines · 2020Article
- DeepScratch: Single-cell based topological metrics of scratch wound assays.Computational and structural biotechnology journal · 2020Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Recently, a robust mechanical method has been established to isolate a small subpopulation of highly tumorigenic tumor repopulating cells (TRCs) from parental melanoma cells. In order to characterize the molecular and mechanical properties of TRCs, we utilized the tension gauge tether (TGT) single-molecule platform and investigated force requirements during early cell spreading events. TRCs required the peak single molecular tension of around 40 pN through integrins for initial adhesion like the parental control cells, but unlike the control cells, they did not spread and formed very few mature focal adhesions (FAs). Single molecule resolution RNA quantification of three Rho GTPases showed that downregulation of Cdc42, but not Rac1, is responsible for the unusual biophysical features of TRCs and that a threshold level of Cdc42 transcripts per unit cell area is required to initiate cell spreading. Cdc42 overexpression rescued TRC spreading through FA formation and restored the sensitivity to tension cues such that TRCs, like parental control cells, increase cell spreading with increasing single-molecular tension cues. Our single molecule studies identified an unusual biophysical feature of suppressed spreading of TRCs that may enable us to distinguish TRC population from a pool of heterogeneous tumor cell population.
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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.