PLOD2 exacerbates cervical squamous cell carcinoma by suppressing p53 by binding to YAP1
Meilin Yin1, Yanhua Weng2, Tianshu Qi1
1Clinical Laboratory Department, Beijing Chaoyang District Maternal and Child Health Care Hospital, Beijing 100021, P.R. China.
Abstract:
Procollagen‑lysine, 2‑oxoglutarate 5‑dioxygenase 2 (PLOD2) has been identified as an oncogene involved in the progression of several human cancers. However, its role in cervical squamous cell carcinoma (CESC) and its underlying mechanisms are not well understood. In the present study, several public databases, RT‑qPCR and western blotting were employed to detect the expression of PLOD2 and the prognosis in CESC. Cell counting kit‑8 assay, wound healing assay, Transwell assay, western blotting and flow cytometry were utilized to assess the proliferation, migration and cell apoptosis of CESC cells. Cellular senescence was examined by RT‑qPCR and β‑galactosidase staining. Prediction of PLOD2 binding to Yes‑associated protein 1 (YAP1) was assessed using BioGrid, HDock and co‑immunoprecipitation, and p53 and p21 signaling were assessed using immunofluorescence staining. The findings indicated that the expression of PLOD2 was elevated in CESC tissues and cell lines, and PLOD2 silencing caused the inhibition of CESC cell proliferation, migration and the promotion of apoptosis and senescence of CESC cells. PLOD2 was predicted to be bound to YAP1 and YAP1 overexpression reversed the effects of PLOD2 silencing on CESC cell proliferation, cell migration, apoptosis and senescence. In addition, PLOD2 facilitated CESC progression by regulating the P53 pathway through YAP1. PLOD2 exerted pro‑oncogenic effects on CESC through the p53 pathway by binding to YAP1. These findings provide new perspectives for the future study of PLOD2‑targeted therapy for CESC.
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