ArticleCancer communications (London, England)2025
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Article in Cancer communications (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Characterizing risk groups in papillary thyroid carcinoma through T-Cell mediated tumor cell killing-related genes: a pathway to therapeutic predictions.European archives of oto-rhino-laryngology : official journal of the European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino-Laryngology - Head and Neck Surgery · 2026Article
- A Quarter Century of EHD Protein Research: From Endosomal Recycling to Ciliopathies.Traffic (Copenhagen, Denmark) · 2026Review
- KAT2A-IGF2BP1-CXCL2 axis in the high lactate tumor microenvironment facilitates resistance to anti-PD-1 therapy in lung adenocarcinoma by recruiting myeloid-derived suppressor cells.Cell death & disease · 2026Article
- WTAP-mediated mMolecular genetics and genomics : MGG · 2026Article
- Bioinformatics profiling of NECTIN4 in lung cancer and comparative evaluation of NECTIN4-targeted ⁶⁸Ga-N188 and ¹⁸F-FDG PET/CT.Journal of translational medicine · 2026Article
- RNA Methylation in Cancer Metabolism: from Mechanisms to Therapeutic Opportunities.International journal of biological sciences · 2026Review
- mCancer communications (London, England) · 2025Article
- Prediction of neoadjuvant therapy efficacy in gastric cancer: the interplay between biomarkers and radiomics and its potential for clinical translation.Frontiers in oncology · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
backgroundEps15 homology domain (EHD) proteins, including EHD1 to EHD4, play vital roles in tumor progression. In this study, we aimed to investigate which specific EHD proteins, if any, are implicated in tumor immune evasion and immunotherapy response.
methodsThe immunotherapy responses of lung adenocarcinoma (LUAD) patients were predicted using tumor immune dysfunction and exclusion (TIDE) analysis. The T cell killing assay was performed by co-culturing activated T cells with LUAD cells. The function of EHD1 as a regulator of programmed death-ligand 1 (PD-L1) endocytic recycling was determined by receptor internalization assays. Methylated RNA immunoprecipitation (MeRIP) was performed to investigate N6-methyladenosine (m
resultsTIDE algorithms and survival analysis identified that EHD1 promoted LUAD immune escape. EHD1 knockdown enhanced T cell cytotoxicity in killing LUAD cells across all effector-to-target (E/T) ratios. EHD1 overexpression exerted the opposite effect. The molecular docking analysis revealed an interaction between EHD1 and the PD-L1 protein, verified by IF and IP. Furthermore, EHD1 knockdown inhibited PD-L1 recycling, thereby promoting its lysosomal degradation. Disruption of the EHD1/PD-L1 interaction impaired the regulatory function of EHD1 in tumor immune evasion. In an immune-competent mouse model, we found that EHD1 silencing impeded tumor immune evasion and enhanced the efficacy of anti‑PD‑1 therapy. MeRIP-qPCR confirmed obvious m
conclusionOur study illuminates the role of m
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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.