Knockdown of GDF15 inhibits endometrial cancer cell proliferation and EMT

Abstract

Endometrial cancer (EC) is a malignant tumor affecting the uterine upper layer. Despite recent advancements, identifying new therapeutic targets remains important for improving patient prognosis. Growth differentiation factor 15 (GDF15) belongs to the Transforming Growth Factor (TGF)-β superfamily and is often upregulated in pathological conditions, including injury and cancers. However, its involvement in EC remains poorly understood. This study aims to elucidate the significance of GDF15 in EC and its potential underlying mechanism. Our results indicate increased GDF15 expression levels in EC tissues, and the knockdown of GDF15 was found to suppress EC cell growth and epithelial-mesenchymal transition (EMT). Moreover, GDF15 depletion inhibited the TGF-β pathway activation. In summary, GDF15 can promote EC cell growth and EMT by modulating the TGF-β/Smad2/Smad3 axis.