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EGF-Upregulated lncRNA ESSENCE Promotes Colorectal Cancer Growth through Stabilizing CAD and Ferroptosis Defense
Xiaoshan Xie1,2,3, Boyu Zhang1,2,3, Jingxuan Peng1,2,3
1Department of General Surgery, The Sixth Affiliated Hospital, Sun Yat-sen University, Guangzhou 510655, China.
Research (Washington, D.C.)
|April 7, 2025
Summary
A newly identified long noncoding RNA, ESSENCE, drives colorectal cancer (CRC) progression by stabilizing the CAD protein and suppressing ferroptosis. Targeting the ESSENCE-CAD pathway offers a novel therapeutic strategy for CRC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Epidermal growth factor receptor/mitogen-activated protein kinase (EGFR/MAPK) signaling is frequently activated in cancers, including colorectal cancer (CRC).
- The roles of long noncoding RNAs (lncRNAs) induced by this pathway in CRC remain largely unknown.
Purpose of the Study:
- To identify and characterize lncRNAs regulated by EGFR/MAPK signaling in CRC.
- To elucidate the oncogenic mechanisms of a novel lncRNA, ESSENCE, in CRC progression.
Main Methods:
- Profiling of lncRNAs induced by EGFR/MAPK signaling.
- Investigating the interaction between ESSENCE, CAD, and KEAP1.
- Assessing the effect of ESSENCE on ferroptosis and CRC cell proliferation.
- Evaluating a combination therapy in a patient-derived xenograft mouse model.
Main Results:
- ESSENCE, a lncRNA mediated by early growth response factor 1, was identified as an oncogenic molecule predicting poor prognosis in CRC.
- ESSENCE directly interacts with CAD, inhibiting its degradation by KEAP1, thereby suppressing ferroptosis and promoting CRC.
- Combined treatment with a MEK inhibitor (selumetinib) and a ferroptosis inducer (sulfasalazine) synergistically inhibited ESSENCE-high CRC in vivo.
Conclusions:
- ESSENCE plays a critical role in CRC progression by stabilizing CAD and inhibiting ferroptosis.
- Targeting the ESSENCE-CAD axis represents a promising therapeutic strategy for CRC.
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