ArticleJournal of cellular physiology2019
NKCC1 promotes EMT-like process in GBM via RhoA and Rac1 signaling pathways.
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- NKCC1: A key regulator of glioblastoma progression.Molecular oncology · 2026Article
- Brain metastases converge on shared geometric architecture and transcriptomic landscape yet remain distinct from gliomas.iScience · 2026Article
- Synthesis of new sulfoximines and sulfonimidamides derivatives as NKCC1 inhibitors.Frontiers in chemistry · 2026Article
- Self-assembled genistein nanoparticles suppress the epithelial-mesenchymal transition in glioblastoma by targeting MMP9.Materials today. Bio · 2025Article
- Detection of circulating tumor cells that predicts the efficacy of neoadjuvant chemotherapy for locally advanced triple-negative breast cancer.Frontiers in medicine · 2025Article
- Exploring the mechanism of triptolide inhibiting the motility of fibroblast-like synoviocytes in rheumatoid arthritis via RhoA/Rho-associated kinase axis, based on network pharmacology, molecular docking and molecular dynamics simulations.Frontiers in pharmacology · 2025Article
- Piezo1, the new actor in cell volume regulation.Pflugers Archiv : European journal of physiology · 2024Review
- Elastocapillary effects determine early matrix deformation by glioblastoma cell spheroids.APL bioengineering · 2024Article
- Article
- Comprehensive analyses of solute carrier family members identify SLC12A2 as a novel therapy target for colorectal cancer.Scientific reports · 2024Article
- Interferon-γ inducible protein 30 promotes the epithelial-mesenchymal transition-like phenotype and chemoresistance by activating EGFR/AKT/GSK3β/β-catenin pathway in glioma.CNS neuroscience & therapeutics · 2023Article
- SPAK-dependent cotransporter activity mediates capillary adhesion and pressure during glioblastoma migration in confined spaces.Molecular biology of the cell · 2023Article
- Proton boron capture therapy (PBCT) induces cell death and mitophagy in a heterotopic glioblastoma model.Communications biology · 2023Article
- Fatostatin induces ferroptosis through inhibition of the AKT/mTORC1/GPX4 signaling pathway in glioblastoma.Cell death & disease · 2023Article
- An update regarding the role of WNK kinases in cancer.Cell death & disease · 2022Review
- Nogo-B promotes invasion and metastasis of nasopharyngeal carcinoma via RhoA-SRF-MRTFA pathway.Cell death & disease · 2022Article
- The NKCC1 ion transporter modulates microglial phenotype and inflammatory response to brain injury in a cell-autonomous manner.PLoS biology · 2022Article
- Rho-GEF Trio regulates osteosarcoma progression and osteogenic differentiation through Rac1 and RhoA.Cell death & disease · 2021Article
- Effect of differential hypoxia-related gene expression on glioblastoma.The Journal of international medical research · 2021Article
- Airway Basal Cells Mediate Hypoxia-Induced EMT by Increasing Ribosome Biogenesis.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma is the most common and lethal primary intracranial tumor. As the key regulator of tumor cell volume, sodium-potassium-chloride cotransporter 1 (NKCC1) expression increases along with the malignancy of the glioma, and NKCC1 has been implicated in glioblastoma invasion. However, little is known about the role of NKCC1 in the epithelial-mesenchymal transition-like process in gliomas. We noticed that aberrantly elevated expression of NKCC1 leads to changes in the shape, polarity, and adhesion of cells in glioma. Here, we investigated whether NKCC1 promotes an epithelial-mesenchymal transition (EMT)-like process in gliomas via the RhoA and Rac1 signaling pathways. Pharmacological inhibition and knockdown of NKCC1 both decrease the expressions of mesenchymal markers, such as N-cadherin, vimentin, and snail, whereas these treatments increase the expression of the epithelial marker E-cadherin. These findings indicate that NKCC1 promotes an EMT-like process in gliomas. The underlying mechanism is the facilitation of the binding of Rac1 and RhoA to GTP by NKCC1, which results in a significant enhancement of the EMT-like process. Specific inhibition or knockdown of NKCC1 both attenuate activated Rac1 and RhoA, and the pharmacological inhibitions of Rac1 and RhoA both impair the invasion and migration abilities of gliomas. Furthermore, we illustrated that NKCC1 knockdown abolished the dissemination and spread of glioma cells in a nude mouse intracranial model. These findings suggest that elevated NKCC1 activity acts in the regulation of an EMT-like process in gliomas, and thus provides a novel therapeutic strategy for targeting the invasiveness of gliomas, which might help to inhibit the spread of malignant intracranial tumors.
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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.