ArticleCancer research2025
Extracellular Domain Shedding of TROP2 Activates EGFR Signaling to Drive Prostate Cancer Metastasis.
Article in Cancer research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed.
- Targeting the ELF1/EGFR/ERK positive feedback loop overcomes resistance to androgen receptor inhibition in AR-Vs positive prostate cancer.Neoplasia (New York, N.Y.) · 2026Article
- Evaluating datopotamab deruxtecan (Dato-DXd) as a novel treatment option for EGFR-mutated non-small cell lung cancer.Future oncology (London, England) · 2026Review
- Innovative use of therapeutic antibodies in lung cancer: the current landscape of ADCs and other antibody-based therapies.Frontiers in oncology · 2026Review
- Feedback regulation between histone H3 lysine 18 lactylation and TROP2-mediated glycolysis drives metastatic progression of colorectal cancer.Clinical and translational medicine · 2026Article
- TROP2 expression in head and neck squamous cell carcinoma: association with the tumor immune microenvironment and clinical outcome.Frontiers in oncology · 2026Article
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
Metastasis is the main cause of prostate cancer-associated deaths, highlighting the urgent need to determine the mechanisms underlying prostate cancer progression. TROP2 (also known as tumor-associated calcium signal transducer 2) is an oncogenic transmembrane surface protein that is highly expressed in metastatic prostate cancer. Naturally occurring cleavage of TROP2 leads to a release of the TROP2 extracellular domain (TECD) into the extracellular environment. In this study, we identified an important functional role of TECD in prostate cancer metastasis. TECD was detectable in media from prostate cancer cells and serum from patients with clinically significant prostate cancer. Although shed TECD did not affect prostate cancer cell proliferation and tumor growth, it increased cell migration and invasion in vitro and promoted metastatic colonization and spontaneous metastasis in vivo. TECD interactome and proteomic studies revealed that TECD binds to EGFR and shed TECD modulates a set of proteins associated with invasion, migration, mTOR signaling, and epithelial-to-mesenchymal transition. Furthermore, elevated shed TECD increased EGFR phosphorylation, resulting in the activation of the EGFR-PI3K-AKT-mTOR pathway in prostate cancer. EGFR inhibitors suppressed the invasive ability of prostate cancer cells driven by TECD overexpression, further supporting the key role of EGFR in TECD-mediated prostate cancer progression. This study uncovers a function of TECD in driving prostate cancer progression and provides mechanistic insights into TECD signaling through EGFR. SIGNIFICANCE: Shed extracellular domain of TROP2 binds to and activates EGFR and stimulates the PI3K-AKT-mTOR signaling cascade to promote prostate cancer metastasis, providing potential biomarkers and therapeutic targets.
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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 Socratic graph.