ArticleCell death & disease2024
PDZK1 suppresses TNBC development and sensitizes TNBC cells to erlotinib via the EGFR pathway.
Article in Cell death & disease, 2024. 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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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.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Beyond conventional therapies: the evolution of targeted agents and immunotherapies in triple-negative breast cancer.Acta pharmacologica Sinica · 2026Review
- Article
- SIRT3 suppresses renal cancer progression by regulating IDH2 acetylation.Scientific reports · 2026Article
- Metal-Organic Frameworks for Precision Phototherapy of Breast Cancer.Molecules (Basel, Switzerland) · 2026Review
- Exosomal POU5 F1 derived from TNBC promotes cancer progression by regulating M2 macrophage polarization via inhibiting TRAF6 ubiquitination and activating AKT in macrophage.Cell biology and toxicology · 2025Article
- PDZK1 inhibits MRP2-mediated oxaliplatin chemosensitivity in hepatocellular carcinoma.Scientific reports · 2025Article
- Microbially produced imidazole propionate impairs prostate cancer progression through PDZK1.Molecular medicine (Cambridge, Mass.) · 2025Article
- Integration of multi-omics profiling reveals an epigenetic-based molecular classification of lung adenocarcinoma: implications for drug sensitivity and immunotherapy response prediction.Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Epidermal growth factor receptor (EGFR)-targeted drugs (erlotinib, etc.) are used to treat multiple types of tumours. EGFR is highly expressed in most triple-negative breast cancer (TNBC) patients. However, only a small proportion of TNBC patients benefit from EGFR-targeted drugs in clinical trials, and the resistance mechanism is unclear. Here, we found that PDZ domain containing 1 (PDZK1) is downregulated in erlotinib-resistant TNBC cells, suggesting that PDZK1 downregulation is related to erlotinib resistance in TNBC. PDZK1 binds to EGFR. Through this interaction, PDZK1 promotes EGFR degradation by enhancing the binding of EGFR to c-Cbl and inhibits EGFR phosphorylation by hindering EGFR dimerisation. We also found that PDZK1 is specifically downregulated in TNBC tissues and correlated with a poor prognosis in TNBC patients. In vitro and in vivo functional assays showed that PDZK1 suppressed TNBC development. Restoration of EGFR expression or kinase inhibitor treatment reversed the degree of cell malignancy induced by PDZK1 overexpression or knockdown, respectively. PDZK1 overexpression sensitised TNBC cells to erlotinib both in vitro and in vivo. In conclusion, PDZK1 is a significant prognostic factor for TNBC and a potential molecular therapeutic target for reversing erlotinib resistance in TNBC cells.
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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.