ArticleResearch (Washington, D.C.)2025
EGF-Upregulated lncRNA ESSENCE Promotes Colorectal Cancer Growth through Stabilizing CAD and Ferroptosis Defense.
Article in Research (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The trial behind it
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Who cites it
4 citing papers in PubMed.
- OTUD6A promotes de novo pyrimidine synthesis by deubiquitinating and stabilizing CAD in cervical cancer.Oncogene · 2026Article
- Article
- CSN6 Promotes Pancreatic Cancer Progression and Gemcitabine Resistance via Antagonizing DCAF1-Mediated Ubiquitination of NPM1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting CAD with a tumor microenvironment-responsive nano-heterojunction for synergistic induction of cuproptosis and inhibition of colorectal cancer progression.Journal of nanobiotechnology · 2025Article
Corrections and comments
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Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidermal growth factor receptor/mitogen-activated protein kinase (EGFR/MAPK) signaling is highly activated in various types of cancer. The long noncoding RNAs induced by this pathway and their roles in colorectal cancer (CRC) have not been fully elucidated. In this study, based on the profiling of long noncoding RNAs triggered by EGFR/MAPK signaling, we identified that ESSENCE (EGF [epidermal growth factor] Signal Sensing CAD's Effect; ENST00000415336), which is mediated by the transcription factor early growth response factor 1, functions as a potent oncogenic molecule that predicts poor prognosis in CRC. Mechanistically, ESSENCE directly interacts with carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase (CAD) and competitively attenuates CAD degradation mediated by its newly discovered E3 ligase KEAP1, thereby suppressing ferroptosis and promoting CRC progression. Importantly, combinational treatment of the mitogen-activated extracellular signal-regulated kinase inhibitor selumetinib and ferroptosis inducer sulfasalazine synergistically suppresses ESSENCE-high CRC in a patient-derived xenograft mouse model. Taken together, these findings demonstrate the crucial role of ESSENCE in mediating CRC progression by regulating CAD stabilization and suggest a therapeutic strategy of targeting the ESSENCE-CAD axis in CRC.
Identifiers
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Registered trials
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