ArticleScientific reports2019
TGFβ-induced cytoskeletal remodeling mediates elevation of cell stiffness and invasiveness in NSCLC.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 41 citations in OpenAlex.
- The miR-16-1-3p suppresses proliferation and invasiveness via the MDM2-p53 axis in TGF-β1 signaling in osteosarcoma.Molecular therapy. Oncology · 2026Article
- Novel tissue mechanics-guided cellular flows drive the formation of feather follicles.The EMBO journal · 2026Article
- Network-based exploration of 4-(phenylsulfonyl)morpholine molecules for metastatic triple-negative breast cancer suppression.PLoS computational biology · 2026Article
- Predominant miRNAs in Animal-Source Foods and Bioinformatic Analysis.Current issues in molecular biology · 2026Article
- Roles of cytoskeleton in metastasis: from its mechanism to therapeutic strategies.Experimental & molecular medicine · 2026Review
- Deciphering the Role of ADAMTS6 in the Epithelial-Mesenchymal Transition of Lung Adenocarcinoma Cells.International journal of molecular sciences · 2025Article
- β-adrenergic signaling modulates breast cancer cell mechanical behaviors through a RhoA-ROCK-myosin II axis.iScience · 2025Article
- A Five-Gene Signature for the Prediction of Event-Free Survival of Both Pediatric and Adult Acute Myeloid Leukemia.Diagnostics (Basel, Switzerland) · 2025Article
- Spatio-temporal transcriptomic analysis reveals distinct nephrotoxicity, DNA damage, and regeneration response after cisplatin.Cell biology and toxicology · 2025Article
- Cellular EMT-status governs contact guidance in an electrospun TACS-mimickingMaterials today. Bio · 2025Article
- Mapping Nanoscale-To-Single-Cell Phosphoproteomic Landscape by Chip-DIA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Research progress on the role of biomechanical clues in the progression of lung cancer.Frontiers in cell and developmental biology · 2025Review
- Article
- The F-actin bundler SWAP-70 promotes tumor metastasis.Life science alliance · 2024Article
- Enigmatic exosomal connection in lung cancer drug resistance.Molecular therapy. Nucleic acids · 2024Review
- Cancer Cell Biomechanical Properties Accompany Tspan8-Dependent Cutaneous Melanoma Invasion.Cancers · 2024Article
- High extracellular glucose promotes cell motility by modulating cell deformability and contractility via the cAMP-RhoA-ROCK axis in human breast cancer cells.Molecular biology of the cell · 2023Article
- Angiogenic signaling pathways and anti-angiogenic therapy for cancer.Signal transduction and targeted therapy · 2023Review
- Nanomechanical Characterization of Ovarian Cancer Cell Lines as a Marker of Response to 2c Treatment.International journal of molecular sciences · 2023Article
- The TT Genotype of theCells · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Importance of growth factor (GF) signaling in cancer progression is widely acknowledged. Transforming growth factor beta (TGFβ) is known to play a key role in epithelial-to-mesenchymal transition (EMT) and metastatic cell transformation that are characterized by alterations in cell mechanical architecture and behavior towards a more robust and motile single cell phenotype. However, mechanisms mediating cancer type specific enhancement of cell mechanical phenotype in response to TGFβ remain poorly understood. Here, we combine high-throughput mechanical cell phenotyping, microarray analysis and gene-silencing to dissect cytoskeletal mediators of TGFβ-induced changes in mechanical properties of on-small-cell lung carcinoma (NSCLC) cells. Our experimental results show that elevation of rigidity and invasiveness of TGFβ-stimulated NSCLC cells correlates with upregulation of several cytoskeletal and motor proteins including vimentin, a canonical marker of EMT, and less-known unconventional myosins. Selective probing of gene-silenced cells lead to identification of unconventional myosin MYH15 as a novel mediator of elevated cell rigidity and invasiveness in TGFβ-stimulated NSCLC cells. Our experimental results provide insights into TGFβ-induced cytoskeletal remodeling of NSCLC cells and suggest that mediators of elevated cell stiffness and migratory activity such as unconventional cytoskeletal and motor proteins may represent promising pharmaceutical targets for restraining invasive spread of lung cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.