Loading
Life sciences · Journal article
Cell Communication and Signaling · October 31, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
The tumor microenvironment (TME) constitutes a distinct biophysical niche that dictates malignancy, extending far beyond a mere structural scaffold. This review outlines the aberrant mechanical properties defining this niche, including solid stress, interstitial fluid pressure (IFP), matrix stiffness, viscoelasticity and microstructure. We describe the mechanotransduction axes from cell-surface mechanosensors and ion channels to the ‘molecular motor-clutch’ machinery that transduce physical cues into nuclear deformation. Furthermore, we discuss the reciprocal crosstalks among cancer cells, cancer-associated fibroblasts (CAFs), and tumor-associated macrophages (TAMs) in restructuring the physical microenvironment. This dynamic remodeling establishes a feed-forward mechanical circuit that sustains proliferation, metastasis, and therapeutic resistance in cancer. Finally, we propose that targeting these biophysical abnormalities to restore mechanical homeostasis represents key therapeutic vulnerabilities for cancer progression.