ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Osteopontin splice variants expression is involved on docetaxel resistance in PC3 prostate cancer cells.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Meta-analysis of Osteopontin splice variants in cancer.BMC cancer · 2023Pooled it
- Review
- Serine/threonine kinase 36 induced epithelial-mesenchymal transition promotes docetaxel resistance in prostate cancer.Scientific reports · 2024Article
- The Multifaceted Role of Osteopontin in Prostate Pathologies.Biomedicines · 2023Review
- Quercetin can be a more reliable treatment for metastatic prostate cancer than the localized disease: An in vitro study.Journal of cellular and molecular medicine · 2023Article
- Osteopontin and Cancer: Insights into Its Role in Drug Resistance.Biomedicines · 2023Review
- Review
- Inducible T-Cell Costimulator Ligand Plays a Dual Role in Melanoma Metastasis upon Binding to Osteopontin or Inducible T-Cell Costimulator.Biomedicines · 2021Article
- Distinctive Prognostic Value and Cellular Functions of Osteopontin Splice Variants in Human Gastric Cancer.Cells · 2021Article
- Inhibition of osteopontin overcomes acquired resistance to afatinib in EGFR-mutant non-small-cell lung cancer.Translational cancer research · 2020Article
- Osteopontin isoforms differentially promote arteriogenesis in response to ischemia via macrophage accumulation and survival.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Cinobufagin Suppresses The Characteristics Of Osteosarcoma Cancer Cells By Inhibiting The IL-6-OPN-STAT3 Pathway.Drug design, development and therapy · 2019Article
- SIRT1 overexpression protects non-small cell lung cancer cells against osteopontin-induced epithelial-mesenchymal transition by suppressing NF-κB signaling.OncoTargets and therapy · 2018Article
- Differential Effects of Autophagy-Related 10 Protein on HCV Replication and Autophagy Flux Are Mediated by Its CysteineFrontiers in immunology · 2018Article
- Human osteopontin: Potential clinical applications in cancer (Review).International journal of molecular medicine · 2017Review
- Osteopontin-a splice variant is overexpressed in papillary thyroid carcinoma and modulates invasive behavior.Oncotarget · 2016Article
- Predictive value of stathmin-1 and osteopontin expression for taxan resistance in metastatic castrate-resistant prostate cancer.Pakistan journal of medical sciencesArticle
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteopontin (OPN) is a phosphoprotein that activates several aspects of tumor progression. Alternative splicing of the OPN primary transcript generates three splicing isoforms, OPNa, OPNb and OPNc. In this report, we investigated some cellular mechanisms by which OPN splice variants could mediate PC3 prostate cancer (PCa) cell survival and growth in response to docetaxel (DXT)-induced cell death. Cell survival before and after DXT treatment was analyzed by phase-contrast microscopy and crystal-violet staining assays. Quantitative real-time PCR and immunocytochemical staining assays were used to evaluate the putative involvement of epithelial-mesenchymal transition (EMT) and OPN isoforms on mediating PC3 cell survival. Upon DXT treatment, PC3 cells overexpressing OPNb or OPNc isoforms showed higher cell densities, compared to cells overexpressing OPNa and controls. Notably, cells overexpressing OPNb or OPNc isoforms showed a downregulated pattern of EMT epithelial cell markers, while mesenchymal markers were mostly upregulated in these experimental conditions. We concluded that OPNc or OPNb overexpression in PC3 cells can mediate resistance and cell survival features in response to DXT-induced cell death. Our data also provide evidence the EMT program could be one of the molecular mechanisms mediating survival in OPNb- or OPNc-overexpressing cells in response to DXT treatment. These data could further contribute to a better understanding of the mechanisms by which PCa cells acquire resistance to DXT treatment.
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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 Socratic graph.