ELF3 (E74 like ETS transcription factor 3) promotes tumor growth and autophagy in pancreatic cancer.

Authors

Yuru Shang, Pingping Zhang, Yanhui Yang, Yibao Fan, Zhichao Yang, Hongshi Sun, Jia Wang, Zhengming Yu, Jiale Wu, Wenxu Wang, Ulf Dietrich Kahlert, Gautam Sethi, Michael Linnebacher, Zhe-Sheng Chen, Daniel J Klionsky, Xianbin Zhang

Published in

Journal of experimental & clinical cancer research : CR. Volume 45. Issue 1. Aug 18, 2026. Epub Aug 18, 2026.

Abstract

Despite the research progress of the past decades, the prognosis for pancreatic ductal adenocarcinoma remains poor. Identifying novel targets and exploring the underlying mechanisms is therefore of great importance. ELF3 (E74 like ETS transcription factor 3) is a member of the E-twenty-six (ETS) family and previous studies suggest that ELF3 may play a promoting role in malignant epithelial tumor; however, the effect and exact mechanism have not been determined in pancreatic cancer.
ELF3 expression and its prognostic relevance in pancreatic cancer were analyzed using clinical datasets. The role of ELF3 in autophagy regulation was evaluated using molecular and cellular approaches in vitro and in vivo. Computer-aided drug design was performed to identify potential ELF3 inhibitors, whose anti-tumor efficacy was subsequently evaluated.
In the present study, it is observed that high expression of ELF3 leads to a poor overall survival in pancreatic cancer patients. Functional experiments demonstrated that knockdown of ELF3 blocks autophagy. In addition, SRT2183 was identified as a potential ELF3 inhibitor using molecular docking. In vitro and in vivo results showed that SRT2183 blocks autophagy and exerts anti-carcinoma effect.
These findings demonstrate that ELF3 promotes autophagy through transcriptional regulation of ATG10 and identify ELF3 as a potential therapeutic target in pancreatic cancer. SRT2183, an ELF3-targeting compound that suppresses autophagic flux and tumor growth, represents a promising candidate for further therapeutic development.

PMID:
43021370
Bibliographic data and abstract were imported from PubMed on 13 Nov 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.