Activating transcription factor 3 inhibits endometrial carcinoma aggressiveness via JunB suppression
- Fangyuan Wang
- Jingjing Li
- Haixia Wang
- Fan Zhang
- Jin Gao
Affiliations: Shanghai Institute of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200127, P.R. China, School of Pharmacy, Shanghai Jiao Tong University, Shanghai 200240, P.R. China, School of Agriculture and Biology, Shanghai Jiao Tong University, Shanghai 200240, P.R. China, Department of Pharmaceutical Sciences, College of Pharmacy and Pharmaceutical Sciences, Washington State University, Spokane, WA 99202, USA
- Published online on: June 19, 2020 https://doi.org/10.3892/ijo.2020.5084
Copyright: © Wang
et al. This is an open access article distributed under the
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The function of activating transcription factor 3 (ATF3) in cancer is context‑dependent and its role in endometrial carcinoma (EC) is yet to be elucidated. In the present study, ATF3 was indicated to be downregulated, while one of the ATF3‑interacting proteins, JunB, was upregulated in ECs according to western blot analysis. After overexpression in ECs, ATF3 inhibited the proliferation and invasion of EC cells and enhanced apoptosis, as well as suppressed the expression of JunB. The properties of EC cells, including the expression of matrix metalloproteinases, tissue inhibitors of metalloproteinases, the cell cycle and apoptosis were all altered by overexpression of ATF3. Furthermore, luciferase activity assay, chromatin precipitation and DNA affinity assay results indicated that ATF3 exerted the aforementioned functions via JunB binding and activator protein‑1 signaling. However, the interaction between ATF3 and JunB did not occur in EC cells under basal conditions, but in ATF3‑overexpressing ECs, which was capable of mitigating EC proliferation, invasion and metastasis. Collectively, the present results suggested that the ATF3/JunB interaction may serve as a potential therapeutic target for ECs.