ArticleOncotarget2017
Caveolin-1-mediated STAT3 activation determines electrotaxis of human lung cancer cells.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- The electrical tumor microenvironment: abnormalities and opportunities.Frontiers in oncology · 2026Review
- Controlling Cell Migratory Patterns Under an Electric Field Regulated by a Neural Network-Based Feedback Controller.Bioengineering (Basel, Switzerland) · 2025Article
- Physiological and pathological roles of caveolins in the central nervous system.Trends in neurosciences · 2024Review
- Glioblastoma U-87 cell electrotaxis is hindered by doxycycline with a concomitant reduction in the matrix metallopeptidase-9 expression.Biochemistry and biophysics reports · 2024Article
- Nanotechnology and Cancer Bioelectricity: Bridging the Gap Between Biology and Translational Medicine.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Tumor treating induced fields: a new treatment option for patients with glioblastoma.Frontiers in neurology · 2024Article
- Direct-Current Electrical Field Stimulation of Patient-Derived Colorectal Cancer Cells.Biology · 2023Article
- Galvanotactic Migration of Glioblastoma and Brain Metastases Cells.Life (Basel, Switzerland) · 2022Article
- Electrotaxis-on-Chip to Quantify Neutrophil Migration Towards Electrochemical Gradients.Frontiers in immunology · 2021Article
- Electric Fields at Breast Cancer and Cancer Cell Collective Galvanotaxis.Scientific reports · 2020Article
- Expression of integrins to control migration direction of electrotaxis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Cell Intrinsic and Extrinsic Mechanisms of Caveolin-1-Enhanced Metastasis.Biomolecules · 2019Review
- LINC81507 act as a competing endogenous RNA of miR-199b-5p to facilitate NSCLC proliferation and metastasis via regulating the CAV1/STAT3 pathway.Cell death & disease · 2019Article
- Doxycycline inhibits electric field-induced migration of non-small cell lung cancer (NSCLC) cells.Scientific reports · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Migration of cancer cells leads to the invasion of distant organs by primary tumors. Further, endogenous electric fields (EFs) in the tumor microenvironment direct the migration of lung cancer cells by a process referred to as electrotaxis - although the precise mechanism remains unclear. Caveolin-1 (Cav-1) is a multifunctional scaffolding protein that is associated with directional cell migration and lung cancer invasion; however, its precise role in lung cancer electrotaxis is unknown. In the present study, we first detected outward electric currents on the tumor body surface in lung cancer xenografts using a highly-sensitive vibrating probe. Next, we found that highly-metastatic H1650-M3 cells migrated directionally to the cathode. In addition, reversal of the EF polarity reversed the direction of migration. Mechanistically, EFs activated Cav-1 and the downstream signaling molecule STAT3. RNA interference of Cav-1 reduced directional cell migration, which was accompanied by dampened STAT3 activation. Furthermore, pharmacological inhibition of STAT3 significantly reduced the electrotactic response, while rescue of STAT3 activation in Cav-1 knock-down cells restored electrotaxis. Taken together, these results suggest that endogenous EFs in the tumor micro-environment might play an important role in lung cancer metastasis by guiding cell migration through a Cav-1/STAT3-mediated signaling pathway.
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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.