Silencing PDCD4 Mediates Transcription Factor EB Overexpression Promoting Proliferation, Migration, and Invasion of Cervical Cancer Hela Cells

Abstract

Cervical cancer is a common gynecologic malignant tumor, the occurrence and development of which are related to multiple genetic and environmental factors. Recent studies have shown that Programmed Cell Death 4 (PDCD4) plays a crucial role in cervical cancer, and that silencing PDCD4 mediates Transcription Factor EB (TFEB) overexpression, promoting cell proliferation, migration, and invasion in this disease. This study utilized the Hela cell line as a cervical cancer model to investigate the changes in TFEB expression levels and the proliferation, migration, invasion, and EMT processes of cervical cancer cells through the silencing of PDCD4. Real-time quantitative PCR and Western blot were employed to assess the expression levels of PDCD4 and TFEB, while CCK-8, scratch assay, Transwell invasion assay, and Western blot were used to evaluate changes in cell proliferation, migration, invasion capabilities, and EMT processes. The experimental results demonstrated that silencing PDCD4 significantly increased the expression level of TFEB. Simultaneously, silencing PDCD4 also significantly accelerated the proliferation rate of Hela cells, enhanced the cells’ migration, invasion capabilities, and promoted the EMT processes. Further experimental results showed that silencing TFEB could partially reverse the promoting effects of PDCD4 silencing on cell proliferation, migration, and invasion. In cervical cancer, silencing PDCD4 can lead to TFEB overexpression, thereby promoting the proliferation, migration, and invasion of Hela cells. These findings provide crucial clues for the in-depth study of molecular mechanisms in cervical cancer and indicate that the PDCD4-TFEB pathway could potentially serve as a target for the treatment and prevention of this disease.