The Mapk-Jun-Tnnt1 Pathway Promotes Proliferation, Metastasis Of Hnscc

To validate the role of TNNT1 in the proliferation, invasion, migration, and cytoskeletal remodeling of tongue cancer. Specific siRNA was used to silence TNNT1 in highly metastatic cells, while a TNNT1 overexpression plasmid was utilized to overexpress the gene in low-metastatic cells. Changes in TNNT1 expression levels were assessed using real-time quantitative PCR and Western blotting techniques. Cell proliferation and self-renewal capabilities were analyzed through CCK8 assays and 3D spheroid formation experiments. Fluorescent probes were employed to detect intracellular calcium ions and mitochondrial membrane potential changes. Colorimetric methods measured intracellular ATP levels and glucose consumption in the culture medium. Wound healing assays, Transwell migration assays, and Matrigel invasion assays evaluated cell invasion and migration abilities. Immunofluorescence staining observed cytoskeletal changes, activation of metastasis-related pathways, and nuclear translocation. CHIP experiments examined the binding of transcription factors to TNNT1, exploring regulatory pathways. TNNT1 promotes epithelial-mesenchymal transition in HNSCC cells, inhibits cell adhesion, regulates cytoskeletal remodeling, and enhances cellular proliferation, invasion, and migration abilities. TNNT1 increases mitochondrial activity in head and neck squamous carcinoma cells, accelerating metabolic processes. The JNK signaling pathway influences TNNT1 expression by regulating phosphorylated c-Jun nuclear translocation, affecting the proliferation and migration of head and neck squamous carcinoma. The MAPK-Jun-TNNT1 pathway promotes the proliferation, self-renewal, migration, and invasion of HNSCC cells, regulates cytoskeletal remodeling, and acts as a pro-oncogenic factor.