ArticleOncoTargets and therapy2019
Osteopontin Mediates Cetuximab Resistance via the MAPK Pathway in NSCLC Cells.
Article in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- The crucial role of SPP1 in osteoporosis, osteoarthritis, and cancer.Pharmaceutical science advances · 2025Review
- Bioinformatics Analysis of Key Genes Associated with Resistance to the Combination of Bevacizumab and Pemetrexed Chemotherapy in Non-small Cell Lung Cancer.Recent patents on anti-cancer drug discovery · 2025Article
- SPP1 expression indicates outcome of immunotherapy plus tyrosine kinase inhibition in advanced renal cell carcinoma.Human vaccines & immunotherapeutics · 2024Article
- Role of osteopontin in cancer development and treatment.Heliyon · 2023Review
- Osteopontin and Cancer: Insights into Its Role in Drug Resistance.Biomedicines · 2023Review
- OPN promotes pro-inflammatory cytokine expression via ERK/JNK pathway and M1 macrophage polarization in Rosacea.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-small cell lung cancer (NSCLC) is the most common type of lung cancer. The high expression of osteopontin (OPN) is an important factor that aggravates drug resistance and causes a poor prognosis in this disease. Therefore, understanding the molecular mechanism of OPN is critical for the treatment and prognosis of NSCLC.
methodsWe used bioinformatics analysis to verify the expression of OPN in normal lung tissues and lung cancer tissues. Then we overexpressed and knocked down OPN in cell lines to detect cell proliferation, migration, invasion, and effects on signaling pathways. Finally, malignant progression and drug resistance induced by OPN were investigated by the wound healing assay, transwell assay, clone formation assay, and Western blot analysis.
resultsWe verified that OPN was upregulated in NSCLC tissues, and its overexpression induced NSCLC cell proliferation, migration, and invasion via the mitogen-activated protein kinase (MAPK) pathway. Furthermore, overexpression of OPN reduced the sensitivity of NSCLC cells to cetuximab by upregulating MAPK pathway-related proteins. These results suggested that OPN promoted malignant progression and mediated drug resistance via the MAPK signaling pathway in NSCLC cells.
conclusionThis study reveals the important role of OPN in NSCLC cells, making it a potential target for improving chemotherapy efficiency in patients with NSCLC.
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