Abstract
Purpose: KLK7, also known as Kallikrein 7, is a secreted enzyme classified as a serine protease. Earlier studies have indicated that KLK7, KLK10, and KLK11 are linked to the survival rates and immune reactions of individuals with papillary thyroid cancer (PTC). This research examines KLK7, investigating its role and expression, and evaluates its viability as a treatment target for PTC. Methods: Initially, we examined the expression and possible functions of KLK7 in PTC using bioinformatics techniques. Researchers examined the impact of KLK7 on the cancer characteristics of PTC and explored if KLK7 influences the Epithelial-mesenchymal transition (EMT) process via the MAPK/ERK pathway in PTC using methods like immunohistochemistry and growth curve analysis. Ultimately, a model using a nude mouse was conducted to confirm the impact of KLK7 on PTC. Results: Our research demonstrated that KLK7 exhibited variations in THCA tissues, and KLK7-related genes had the role of participating in protein synthesis, genetic variation, mRNA degradation and immune microenvironment of PTC. KLK7 was upregulated in PTC tissues and positively associated with clinical stage and lymph node metastasis. Furthermore, the inhibition of KLK7 significantly diminished the proliferation, migration, and invasiveness of PTC cells. Notably, silencing KLK7 reduced phosphorylation of ERK1/2 and suppression of EMT. In vivo experiments further supported these findings. KLK7 might serve as an efficacious therapeutic target and predictive biomarker for PTC patients. Conclusion: KLK7 could be essential in the cancerous advancement of PTC by influencing the EMT via the MAPK/ERK signaling pathway, thereby impacting the growth, migration, and invasiveness of PTC cells. KLK7 appears to be a promising candidate for targeting in PTC therapy.