Piezo mechanosensitive channels: A biological hub for intestinal barrier homeostasis and an emerging target for disease intervention

Table 4 Pathogenic mechanisms of piezo in colon cancer

Pathogenic mechanism	Related pathways	Specific effect
Tumor promotion	Piezo1 gene functional mutation increases cancer risk[92]	Promotes the transformation of normal mucosal epithelium into adenoma and accelerates the malignant progression from adenoma to carcinoma
Tumor proliferation and metastasis	Piezo2 drives the proliferation, migration, and angiogenesis of colon cancer cells by activating the SLIT2/ROBO1 pathway, which upregulates HIF-1α/VEGFC, and collaborates with CAFs to shape the pro-oncogenic microenvironment[93]	Accelerated tumor progression, significantly increased rates of lymph node metastasis and distant metastasis risk, and decreased overall patient survival rate
	Piezo1 induces EMT and angiogenesis by activating the Ca2+ influx/HIF-1α/VEGF signaling axis[94]	Tumor cell proliferation and migration
Tumor immune evasion	Piezo1 activation downregulates MCU, upregulates HIF-1α and VEGF, disrupts mitochondrial function, and promotes cancer cell metastasis[92]	Enhances tumor cell proliferation and migration, resulting in poor patient prognosis
	By regulating Piezo1 to influence Ca2+ levels, activate or degrade NFAT1, and maintain the stem cell characteristics of colon cancer[95]	Tumor development and immune evasion

SLIT2: Slit homolog 2; ROBO1: Roundabout homolog 1; HIF-1α: Hypoxia-inducible factor 1-alpha; VEGFC: Vascular endothelial growth factor C; CAFs: Cancer-associated fibroblasts; EMT: Epithelial-mesenchymal transition; VEGF: Vascular endothelial growth factor; MCU: Mitochondrial calcium uniporter; NFAT1 Nuclear factor of activated T-cells 1.