ArticleInternational dental journal2026
Matrix Stiffness Drives Aggressive Phenotype in Tongue Squamous Cell Carcinoma via Mechanotransduction-Stromal Signalling.
Article in International dental journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesTongue squamous cell carcinoma (TSCC) is a highly aggressive malignancy where extracellular matrix (ECM) stiffening drives epithelial-mesenchymal transition (EMT). However, the specific mechanotransduction pathways and the distinction between primary and metastatic cell responses remain insufficiently defined. This study investigated how substrate stiffness regulates TSCC progression via a dual-regulatory mechanism: direct cell-intrinsic mechanotransduction and indirect stromal paracrine signalling.
methodsTwo human TSCC cell lines with distinct origins, HSC-4 (metastatic) and HSC-7 (primary), were cultured on tunable collagen-coated polydimethylsiloxane (PDMS) substrates of varying stiffness (soft and stiff). Cell morphology, migration, proliferation, EMT marker expression, integrin and YAP expressions were assessed using wound healing assays, qRT-PCR and immunofluorescence staining. The involvement of actin cytoskeleton was examined using cytochalasin D. Additionally, the paracrine effects were evaluated by culturing TSCC cells with conditioned media from gingival fibroblasts (HGF-CM) cultured on different substrate stiffness.
resultsStiff substrates induced elongated, mesenchymal-like morphology and significantly enhanced migration in TSCC cells. Increased stiffness also upregulated EMT-associated markers (CDH2, VIM, MMP2), while induced YAP nuclear translocation and increased mechanosensitive integrin expression. Disruption of the actin cytoskeleton with cytochalasin D suppressed this stiffness-induced EMT marker expressions, indicating that cytoskeletal tension mediates mechanotransduction. Furthermore, HGF-CM derived from stiff substrates significantly upregulated EMT-related expression in HSC cells.
conclusionsMatrix stiffness drives TSCC progression through a dual mechanism: direct actin-mediated and YAP-associated mechanotransduction and indirect stiffness-modulated fibroblast signalling. These findings highlight that mechanical cues in the tumour microenvironment differentially regulate primary and metastatic phenotypes in TSCC. CLINICAL SIGNIFICANCE: Mechanical properties of the tumour microenvironment drive TSCC progression, suggesting that ECM stiffness is likely to be associated with altered TSCC phenotypes, providing a basis for future mechanobiology-focused studies on TSCC progression and management.
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.