ArticleOncology reports2019
TROP2 promotes the proliferation and metastasis of glioblastoma cells by activating the JAK2/STAT3 signaling pathway.
Article in Oncology reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 73 citations in OpenAlex.
- 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
- Angiotensin II Receptor-Associated Protein (AGTRAP) Enhances Glioma Cell Survival Through the IL-6/JAK2/STAT3 Pathway and Correlates With an Immunosuppressive Microenvironment.CNS neuroscience & therapeutics · 2026Article
- Emerging Targeted and Multimodal Therapeutic Strategies in Breast Cancer: A Comprehensive Review.Breast cancer (Dove Medical Press) · 2026Review
- [Trop-2 expression in solid tumors : Expanded protein diagnostics within the molecular tumor board].Pathologie (Heidelberg, Germany) · 2025Article
- Near-Infrared Photoimmunotherapy in Brain Tumors-An Unexplored Frontier.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Exploring the Role of ADCs in Brain Metastases and Primary Brain Tumors: Insight and Future Directions.Cancers · 2025Review
- The dual HDAC/PI3K inhibitor CUDC-907 inhibits the growth and proliferation of MYC-driven Group 3 medulloblastoma.Cell death discovery · 2025Article
- Trop-2 expression in non-small cell lung cancer.PloS one · 2025Article
- TROP2: as a promising target in lung cancer.Frontiers in oncology · 2025Review
- Novel Anti-Trop2 Nanobodies Disrupt Receptor Dimerization and Inhibit Tumor Cell Growth.Pharmaceutics · 2024Article
- TROP2 is highly expressed in triple-negative breast cancer CTCs and is a potential marker for epithelial mesenchymal CTCs.Molecular therapy. Oncology · 2024Article
- An assembly of TROP2-mediated signaling events.Journal of cell communication and signaling · 2023Article
- Sanggenon C inhibits cell proliferation and induces apoptosis by regulating the MIB1/DAPK1 axis in glioblastoma.MedComm · 2023Article
- CAR T cells equipped with a fully human scFv targeting Trop2 can be used to treat pancreatic cancer.Journal of cancer research and clinical oncology · 2022Article
- Selection of Payloads for Antibody-Drug Conjugates Targeting Ubiquitously Expressed Tumor-Associated Antigens: a Case Study.The AAPS journal · 2022Article
- Deoxyelephantopin Induces Apoptosis and Enhances Chemosensitivity of Colon Cancer via miR-205/Bcl2 Axis.International journal of molecular sciences · 2022Article
- MOXD1 knockdown suppresses the proliferation and tumor growth of glioblastoma cells via ER stress-inducing apoptosis.Cell death discovery · 2022Article
- ZC3H15 promotes gastric cancer progression by targeting the FBXW7/c-Myc pathway.Cell death discovery · 2022Article
- A New Kid on the Block: Sacituzumab Govitecan for the Treatment of Breast Cancer and Other Solid Tumors.Molecules (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trophoblast cell surface antigen 2 (TROP2), a single transmembrane domain protein, is often found to be highly expressed in various types of human cancers. However, the biological function and molecular mechanism of TROP2 in glioblastoma have not been fully elucidated, particularly in regards to cell proliferation and metastasis of glioblastoma cells. In the present study, it was demonstrated that TROP2 expression was increased in glioblastoma tissues and glioblastoma cell lines by immunohistochemical analysis and western blot analysis. High TROP2 expression was significantly correlated with the poor survival of glioblastoma patients. MTT assay, BrdU incorporation assay, flow cytometry and Transwell assay were performed to demonstrate that knockdown of TROP2 in glioblastoma cells inhibited cell proliferation and metastasis. We found that the effects of TROP2‑knockdown on glioblastoma cells were associated with the inhibition of JAK2 and STAT3 phosphorylation and decreased transcription of STAT3 target genes. In addition, blocking the activation of JAK2/STAT3 signaling by WP1066 negated the effects of TROP2 overexpression. Furthermore, exogenous IL‑6, which functions as a potent activator of JAK2/STAT3 signaling, was able to rescue the phosphorylation of JAK2 and STAT3 in TROP2‑silenced glioblastoma cells and regulate phenotypic changes in these cells. Therefore, we revealed a novel mechanism by which TROP2 activates the JAK2/STAT3 pathway to promote the growth and metastasis of glioblastoma cells. These data offer insight into the function of TROP2 in glioblastoma and indicate that TROP2 is a promising biomarker and therapeutic target for glioblastoma patients.
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