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Published on: August 2, 2024
PACT Inhibits Malignant Biological Behavior of Ovarian Cancer Cells by Regulating TERT Expression
Xuemei Yang1,2, Qian Zhang3, Xiaofeng Yang1
1Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Molecular Carcinogenesis
|July 16, 2026
Summary
p53-associated cellular protein-testes derived (PACT) promotes ovarian cancer (OC) progression by inhibiting ferroptosis. Targeting PACT may offer a new therapeutic strategy for OC by reactivating ferroptosis and suppressing tumor growth.
Area of Science:
- Oncology
- Cell Biology
- Biochemistry
Background:
- Ovarian cancer (OC) is a deadly malignancy with few effective treatments.
- The role of p53-associated cellular protein-testes derived (PACT) in OC and ferroptosis is not well understood.
Purpose of the Study:
- To investigate the function of PACT in OC cell proliferation, migration, invasion, and ferroptosis.
- To elucidate the molecular mechanisms underlying PACT's role in OC progression, focusing on the Keap1-Nrf2-TERT pathway.
Main Methods:
- siRNA-mediated knockdown and overexpression of PACT in OC cell lines (A2780, OVCAR-3).
- Assays for cell proliferation (CCK-8), migration/invasion (Transwell), and ferroptosis (cell death, iron, MDA, ROS, SLC7A11, GPX4).
- Co-immunoprecipitation, ubiquitination assays, subcellular localization analysis, and in vivo xenograft models.
Main Results:
- PACT knockdown inhibited OC cell proliferation, migration, and invasion while promoting ferroptosis.
- PACT promotes OC progression by suppressing ferroptosis via the Keap1-Nrf2-TERT pathway, enhancing TERT expression and telomerase activity.
- PACT facilitates Keap1 ubiquitination and degradation, promoting Nrf2 nuclear translocation and subsequent TERT upregulation.
Conclusions:
- PACT drives ovarian cancer progression by suppressing ferroptosis and promoting malignant phenotypes through the Keap1-Nrf2-TERT axis.
- Targeting PACT is a potential therapeutic strategy for ovarian cancer.
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