ArticleEMBO molecular medicine2012
TROP2 is epigenetically inactivated and modulates IGF-1R signalling in lung adenocarcinoma.
Article in EMBO molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 115 citations in OpenAlex.
- Anti-TROP2 Antibody Drug Conjugates in EGFR-Mutant Non-Small Cell Lung Cancer: Biological Rationale and Clinical Challenges.Pharmaceutics · 2026Review
- TROP2 Is Uniformly Expressed in Primary Prostate Cancer but Frequently Reduced in Recurrent Disease.Cancers · 2026Article
- Bimodality in pan-cancer proteomics reveals new opportunities for biomarker discovery.Genome biology · 2026Article
- [European journal of nuclear medicine and molecular imaging · 2026Article
- Quantitative Assays for TROP2 Measurement in Breast Cancer and Comparison to H-Score.Applied immunohistochemistry & molecular morphology : AIMM · 2026Article
- From biology to the clinic: research evidence and therapeutic advances of TROP2-targeted antibody-drug conjugates in small cell lung cancer.Translational lung cancer research · 2026Review
- TROP2/claudin program mediates immune exclusion to impede checkpoint blockade in breast cancer.Journal for immunotherapy of cancer · 2026Article
- Cellular landscape and diagnostic value of TROP2 in cerebrospinal fluid of lung adenocarcinoma leptomeningeal metastases.NPJ precision oncology · 2026Article
- The emerging role of TROP2 as a diagnostic and prognostic biomarker in bladder tumor.Cancer cell international · 2026Review
- Feedback regulation between histone H3 lysine 18 lactylation and TROP2-mediated glycolysis drives metastatic progression of colorectal cancer.Clinical and translational medicine · 2026Article
- METTL3-mediated m6A modification of TACSTD2 mRNA inhibits papillary thyroid cancer progression by activating the TNF signaling and blocking epithelial-mesenchymal transition.Scientific reports · 2025Article
- Engineered Nanobody-Bearing Extracellular Vesicles Enable Precision Trop2 Knockdown in Resistant Breast Cancer.Pharmaceutics · 2025Article
- The Mode of Action and Clinical Outcomes of Sacituzumab Govitecan in Solid Tumors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2025Review
- Emerging evidence of targeting non-oncogenic drivers for gastric cancer: Claudin18.2 and beyond.Therapeutic advances in medical oncology · 2025Review
- Comparative immunohistochemical expression of TROP2 in brain metastatic and primary tumors.American journal of cancer research · 2025Article
- TROP2: as a promising target in lung cancer.Frontiers in oncology · 2025Review
- The tricky effects of TROP2 in lung cancer: from clinical practice back to fundamental investigations.Frontiers in oncology · 2025Review
- Unlocking the potential of antibody-drug conjugates in cervical cancer: emerging targets and clinical trials.Frontiers in pharmacology · 2025Review
- Novel Anti-Trop2 Nanobodies Disrupt Receptor Dimerization and Inhibit Tumor Cell Growth.Pharmaceutics · 2024Article
- Trop2-targeted therapy in breast cancer.Biomarker research · 2024Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trop-2, a cell surface glycoprotein, contains both extracellular epidermal growth factor-like and thyroglobulin type-1 repeat domains. Low TROP2 expression was observed in lung adenocarcinoma tissues as compared with their normal counterparts. The lack of expression could be due to either the loss of heterozygosity (LOH) or hypermethylation of the CpG island DNA of TROP2 upstream promoter region as confirmed by bisulphite sequencing and methylation-specific (MS) polymerase chain reaction (PCR). 5-Aza-2'-deoxycytidine treatment on lung cancer cell (CL) lines, CL1-5 and A549, reversed the hypermethylation status and elevated both TROP2 mRNA and protein expression levels. Enforced expression of TROP2 in the lung CL line H1299 reduced AKT as well as ERK activation and suppressed cell proliferation and colony formation. Conversely, silencing TROP2 with shRNA transfection in the less efficiently tumour-forming cell line H322M enhanced AKT activation and increased tumour growth. Trop-2 could attenuate IGF-1R signalling-mediated AKT/β-catenin and ERK activation through a direct binding of IGF1. In conclusion, inactivation of TROP2 due to LOH or by DNA methylation may play an important role in lung cancer tumourigenicity through losing its suppressive effect on IGF-1R signalling and tumour growth.
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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.