1. Academic Validation
  2. BET inhibitor JQ1 induces apoptosis of ovarian and endometrial endometrioid carcinoma cells by downregulating c‑Myc

BET inhibitor JQ1 induces apoptosis of ovarian and endometrial endometrioid carcinoma cells by downregulating c‑Myc

  • Oncol Lett. 2024 Dec 19;29(3):106. doi: 10.3892/ol.2024.14852.
Saki Tanimoto 1 Kenbun Sone 1 Yuri Jonouchi 1 Ryuta Hachijo 1 Eri Suzuki 1 Natsumi Tsuboyama 1 Yusuke Toyohara 1 Futaba Inoue 1 Harunori Honjoh 1 Tomohiko Fukuda 1 Ayumi Taguchi 1 Yuichiro Miyamoto 1 Takayuki Iriyama 1 Mayuyo Mori 1 Ken Asada 2 3 Masaaki Komatsu 2 3 Syuzo Kaneko 2 3 Ryuji Hamamoto 2 3 Osamu Wada-Hiraike 1 Katsutoshi Oda 4 Yasushi Hirota 1 Yutaka Osuga 1
Affiliations

Affiliations

  • 1 Department of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
  • 2 Division of Medical AI Research and Development, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
  • 3 Cancer Translational Research Team, RIKEN Center for Advanced Intelligence Project, Tokyo 103-0027, Japan.
  • 4 Division of Integrated Genomics, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Abstract

Although ovarian endometrioid carcinoma (OEC), frequently associated with endometrial endometrioid carcinoma (EEC), is often diagnosed at an early stage, the prognosis remains poor. The development of new, effective drugs to target these cancers is highly desirable. The bromodomain and extra-terminal domain (BET) family proteins serve a role in regulating transcription by recognizing histone acetylation, which is implicated in several types of Cancer. BET inhibitors have been reported as promising Cancer drugs. The present study aimed to assess the role of JQ1, a BET inhibitor, in ovarian and endometrial cancers. The sensitivity of OEC and EEC cell lines to JQ1 was assessed using cell viability and colony formation assays. Additionally, western blotting and cell cycle assays were performed to evaluate changes in c-Myc expression and Apoptosis markers. Cell proliferation and colony formation assays revealed significant tumor suppression in both OEC and EEC cell lines in response to JQ1 treatment. Furthermore, treatment with JQ1 induced a decrease in c-Myc expression and an increase in Apoptosis markers, such as cleaved PARP and the cell population in the sub-G1 phase, in both OEC and EEC cell lines. The findings of the present study indicate that JQ1 may induce cell death through c-Myc inhibition and could be a potentially novel therapeutic agent in the treatment in OEC and EEC. However, the direct mechanism, has not been fully elucidated, warranting further investigation.

Keywords

apoptosis; bromodomain and extra-terminal domain protein; c-Myc; endometrioid endometrial carcinoma; epigenetics; ovarian endometrioid carcinoma.

Figures
Products