ArticleRadiation oncology (London, England)2015
Influence of hypoxia and irradiation on osteopontin expression in head and neck cancer and glioblastoma cell lines.
Article in Radiation oncology (London, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Matricellular proteins: Potential biomarkers in head and neck cancer.Journal of cell communication and signaling · 2024Review
- The value of plasma hypoxia markers for predicting imaging-based hypoxia in patients with head-and-neck cancers undergoing definitive chemoradiation.Clinical and translational radiation oncology · 2022Article
- Differences in stem cell marker and osteopontin expression in primary and recurrent glioblastoma.Cancer cell international · 2022Article
- Association of Notch-1, osteopontin and stem-like cells in ENU-glioma malignant process.Oncotarget · 2018Article
- Periarteriolar Glioblastoma Stem Cell Niches Express Bone Marrow Hematopoietic Stem Cell Niche Proteins.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2018Article
- Tumor Acidosis and Hypoxia Differently Modulate the Inflammatory Program: Measurements In Vitro and In Vivo.Neoplasia (New York, N.Y.) · 2017Article
- Cancer stem cells (CSCs), cervical CSCs and targeted therapies.Oncotarget · 2017Review
- Implications of Hypoxia in Breast Cancer Metastasis to Bone.International journal of molecular sciences · 2016Review
- New role of osteopontin in DNA repair and impact on human glioblastoma radiosensitivity.Oncotarget · 2016Article
- TGFβ3-mediated induction of Periostin facilitates head and neck cancer growth and is associated with metastasis.Scientific reports · 2016Article
- Simultaneous perturbation of the MAPK and the PI3K/mTOR pathways does not lead to increased radiosensitization.Radiation oncology (London, England) · 2015Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor hypoxia is a known risk factor for reduced response to radiotherapy. The evaluation of noninvasive methods for the detection of hypoxia is therefore of interest. Osteopontin (OPN) has been discussed as an endogenous hypoxia biomarker. It is overexpressed in many cancers and is involved in tumor progression and metastasis.
methodsTo examine the influence of hypoxia and irradiation on osteopontin expression we used different cell lines (head and neck cancer (Cal27 and FaDu) and glioblastoma multiforme (U251 and U87)). Cells were treated with hypoxia for 24 h and were then irradiated with doses of 2 and 8 Gy. Osteopontin expression was analyzed on mRNA level by quantitative real-time RT-PCR (qPCR) and on protein level by western blot. Cell culture supernatants were evaluated for secreted OPN by ELISA.
resultsHypoxia caused an increase in osteopontin protein expression in all cell lines. In Cal27 a corresponding increase in OPN mRNA expression was observed. In contrast the other cell lines showed a reduced mRNA expression under hypoxic conditions. After irradiation OPN mRNA expression raised slightly in FaDu and U87 cells while it was reduced in U251 and stable in Cal27 cells under normoxia. The combined treatment (hypoxia and irradiation) led to a slight increase of OPN mRNA after 2 Gy in U251 (24 h) and in U87 (24 and 48 h) cell lines falling back to base line after 8 Gy. This effect was not seen in Cal27 or in FaDu cells. Secreted OPN was detected only in the two glioblastoma cell lines with reduced protein levels under hypoxic conditions. Again the combined treatment resulted in a minor increase in OPN secretion 48 hours after irradiation with 8 Gy.
conclusionOsteopontin expression is strongly modulated by hypoxia and only to a minor extent by irradiation. Intracellular OPN homeostasis seems to vary considerably between cell lines. This may explain the partly conflicting results concerning response prediction and prognosis in the clinical setting.
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