ArticleScientific reports2018
Optogenetic control of epithelial-mesenchymal transition in cancer cells.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Illuminating cancer therapy: The translational path of optogenetics.Bioactive materials · 2026Review
- Protocol for optogenetic stimulation of cells under physical confinement.STAR protocols · 2026Article
- Optogenetic manipulation of estrogen receptor signaling to improve estrogen deficiency.iScience · 2026Article
- Oncogenic Alterations in PI3K Signaling Emulated Optogenetically Recapitulate Some Phenotypic Changes in Mammary Epithelia.ACS synthetic biology · 2026Article
- Optogenetics for Investigating and Targeting Hallmark Traits of Cancer.Biomolecules · 2026Review
- Engineered In Vitro Platforms for Mechanochemical Control of Cell Migration.Cold Spring Harbor perspectives in biology · 2025Review
- POT, an optogenetics-based endogenous protein degradation system.Communications biology · 2025Article
- Femtosecond-laser stimulation induces senescence of tumor cellsBiomedical optics express · 2022Article
- Cellular Plasticity during Metastasis: New Insights Provided by Intravital Microscopy.Cold Spring Harbor perspectives in medicine · 2020Review
- Epigenetic feedback and stochastic partitioning during cell division can drive resistance to EMT.Oncotarget · 2020Article
- Frontiers in Intravital Multiphoton Microscopy of Cancer.Cancer reports (Hoboken, N.J.) · 2020Review
- Techniques for Studying Decoding of Single Cell Dynamics.Frontiers in immunology · 2019Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Epithelial-mesenchymal transition (EMT) is one of the most important mechanisms in the initiation and promotion of cancer cell metastasis. The phosphoinositide 3-kinase (PI3K) signaling pathway has been demonstrated to be involved in TGF-β induced EMT, but the complicated TGF-β signaling network makes it challenging to dissect the important role of PI3K on regulation of EMT process. Here, we applied optogenetic controlled PI3K module (named 'Opto-PI3K'), which based on CRY2 and the N-terminal of CIB1 (CIBN), to rapidly and reversibly control the endogenous PI3K activity in cancer cells with light. By precisely modulating the kinetics of PI3K activation, we found that E-cadherin is an important downstream target of PI3K signaling. Compared with TGF-β treatment, Opto-PI3K had more potent effect in down-regulation of E-cadherin expression, which was demonstrated to be regulated in a light dose-dependent manner. Surprisingly, sustained PI3K activation induced partial EMT state in A549 cells that is highly reversible. Furthermore, we demonstrated that Opto-PI3K only partially mimicked TGF-β effects on promotion of cell migration in vitro. These results reveal the importance of PI3K signaling in TGF-β induced EMT, suggesting other TGF-β regulated signaling pathways are necessary for the full and irreversible promotion of EMT in cancer cells. In addition, our study implicates the great promise of optogenetics in cancer research for mapping input-output relationships in oncogenic pathways.
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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.