ArticleMolecular oncology2026
Targeting the EpCAM-AXL axis to overcome drug resistance in lung cancer.
Article in Molecular oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Drug resistance significantly limits the long-term effectiveness of targeted therapies in lung cancer. AXL, a receptor tyrosine kinase (RTK), is a well-established driver of drug resistance in many cancers, including lung cancer. Epithelial cell adhesion molecule (EpCAM), which is commonly overexpressed in epithelial cancers, is also a critical signaling molecule. In this study, we elucidated the role of EpCAM in drug resistance and its mechanistic association with AXL. We found that soluble epithelial cell adhesion molecule (sEpCAM) expression robustly enhanced hallmark cancer phenotypes and promoted pro-survival functions by upregulating AXL expression. Gene expression and pathway analyses further identified significant alterations in core cancer signaling pathways, including NF-kB, STAT3, AKT, and ERK. The ectopic expression of sEpCAM concurrently upregulated endogenous EpCAM expression in the tumor environment. Functionally, sEpCAM confers broad resistance to conventional chemotherapy. Drug sensitivity assays revealed that proteasome inhibition effectively reversed the sEpCAM-induced drug resistance by reducing AXL protein levels. Translational analysis of the lung cancer patient cohort data indicated that patients with aggressive disease co-expressing EpCAM and AXL may be particularly amenable to proteasome-based therapy. Characterization of the EpCAM-AXL axis gene signature further uncovered connections to p53, integrin, and Rho GTPase signaling as well as an intriguing link to tumor immune evasion. Our findings suggest that EpCAM-AXL co-expression in a subset of patients with lung cancer serves as both a predictive biomarker and a promising therapeutic target to counteract treatment failure.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.