ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Pharmacology of Anti-Cancer Drugs
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1634995
BCL6 Promotes the Progression of High-Grade Serous Ovarian Cancer Cells by Inhibiting PLAAT4
Provisionally accepted
- 1The First Affiliated Hospital of University of Science and Technology of China, Hefei, China
- 2Anhui University of Chinese Medicine, Hefei, China
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Background B-cell lymphoma 6 (BCL6) is increasingly recognized as a driver of cancer progression; however, the precise molecular mechanisms by which BCL6 facilitates high-grade serous ovarian cancer (HGSOC) progression remain incompletely understood. Methods In this study, immunohistochemical (IHC) staining was used to evaluate the expression of BCL6 and PLAAT4 in HGSOC tissues and normal tissues. Cleavage under targets and tagmentation (CUT&Tag) was combined with RNA sequencing (RNA-seq) analyses to screen and identify the downstream regulatory mechanisms of BCL6. Wound healing assays, plate cloning, EdU, and transwell assays were used to analyze cell proliferation and invasion. The expression of PI3K-AKT, EMT, and proliferation markers were analyzed by immunohistochemistry in vivo or by western blot in vitro. In vivo, we established a subcutaneous transplantation tumor model and abdominal metastasis model in nude mice to verify the role of BCL6 and PLAAT4 in HGSOC progression. Results Clinical analyses revealed that BCL6 expression is significantly elevated in high-grade serous ovarian cancer (HGSOC) tissues compared with that in normal tissues, whereas PLAAT4 expression is reduced. Moreover, high BCL6 and low PLAAT4 expression are associated with poor prognosis in patients with HGSOC. Biological function tests showed that BCL6 contributes to tumor cell proliferation, invasion, and migration, and plays an important role in the progression of HGSOC in vivo. Mechanistically, our investigation revealed that BCL6 promotes HGSOC progression by downregulating PLAAT4, thereby influencing the activation of the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. Conclusions Collectively, these findings elucidate the pivotal role of the BCL6-PLAAT4-AKT axis in HGSOC progression, establishing a molecular framework for targeting this pathway as a potential therapeutic strategy against HGSOC.
Keywords: BCL6, PLAAT4, high-grade serous ovarian cancer, Akt, ovarian cancer
Received: 25 May 2025; Accepted: 25 Jun 2025.
Copyright: © 2025 Wan, Zhao, Chen, Peng and Tao. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Jinhui Tao, The First Affiliated Hospital of University of Science and Technology of China, Hefei, China
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