Novel role of the lncRNA EPR as oncosuppressor in intestinal cancer
We previously reported that the murine lncRNA Epr is essential for maintaining colon mucosal integrity and permeability. Mice lacking Epr in the colon are more vulnerable to colitis and tumor development. Additionally, we demonstrated that human EPR expression is reduced in ulcerative colitis and in a small cohort of colon adenocarcinoma patients. Here, we present evidence that human and mouse EPR share several key physiological features: preferential binding to the KH1 domain of their interacting protein, KSRP; specific expression in canonical and immature goblet cells of the large intestine; and a functional role in intestinal goblet cell development. The correlation between EPR levels and survival in large cohorts of metastatic colon adenocarcinoma patients, combined with the capacity of human EPR to inhibit cell proliferation and induce apoptosis in two distinct human colon adenocarcinoma cell lines, suggests that EPR may serve as both a valuable prognostic marker for goblet cell-derived adenocarcinomas and a potential therapeutic target.
Authors
- Ettore Zapparoli (ORCID: https://orcid.org/0000-0003-4170-7902)
- Maira Rossi (ORCID: https://orcid.org/0000-0001-8199-4999)
- Luca Caputo (ORCID: https://orcid.org/0000-0002-1697-9968)
- Prem Puri (ORCID: https://orcid.org/0000-0003-4964-0095)
- Roberto Gherzi (ORCID: https://orcid.org/0000-0001-8654-0611)
- Paola Briata (ORCID: https://orcid.org/0000-0001-8456-7618)
- Monica Nicolau (ORCID: https://orcid.org/0009-0004-6534-1874)
- Jesus R Barajas
- Naomi Shim
Institutions
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Discovery Institute (US)
- San Diego City College (US)
- Ospedale Policlinico San Martino (IT)
- San Diego Unified School District (US)
- University of Turin (IT)
Publication Details
- Journal
- bioRxiv (Cold Spring Harbor Laboratory)
- Published
- 2026-05-01
- DOI
- https://doi.org/10.64898/2026.04.28.719975
- Primary Topic
- Cancer-related molecular mechanisms research
- Type
- article
- Field-Weighted Citation Impact
- 0.00