ArticlePathology oncology research : POR2020
Mutation and Expression of a Candidate Tumor Suppressor Gene EPB41L3 in Gastric and Colorectal Cancers.
Article in Pathology oncology research : POR, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- EPB41L3 Inhibits the Progression of Cervical Cancer Via the ERK/p38 MAPK Signaling Pathway.Molecular biotechnology · 2025Article
- Prognostic role and tumor-suppressive effects of CADM family members and the potential molecular mechanisms of CADM1 in neuroblastoma.Discover oncology · 2025Article
- Expression and hypermethylation of JAM and EPB41L3 in cervical squamous cell carcinoma: Clinical significance and applications.Histology and histopathology · 2024Article
- Digital spatial profiling of human parathyroid tumors reveals cellular and molecular alterations linked to vitamin D deficiency.PNAS nexus · 2023Article
- Cytological DNA methylation for cervical cancer screening: a validation set.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Erythrocyte Membrane Protein Band 4.1 Like 3 (EPB41L3) is candidate tumor suppressor gene (TSG) in various cancers. EPB41L3 downregulation has been identified in many solid cancers including gastric (GC) and colorectal cancers (CRCs), but somatic inactivating mutation along with protein expression in cancers are largely unexplored. The aim of our study was to find whether EPB41L3 gene was mutated and expressionally altered in GC and CRC. EPB41L3 gene has a mononucleotide repeat in the coding sequence that could be mutated in cancers with high microsatellite instability (MSI-H). We analyzed 79 GCs and 124 CRCs, and found that only one CRC with MSI-H (1.3%) harbored the frameshift mutation within the repeat. In immunohistochemistry, loss of EPB41L3 expression was identified in 49% of GCs and 42% of CRCs. Our data may indicate EPB41L3 that loss of expression but not frameshift mutation may play a role in GC and CRC development by inhibiting TSG functions of EPB41L3.
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Registered trials
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