ArticlePloS one2013
Inhibition of β2-microglobulin/hemochromatosis enhances radiation sensitivity by induction of iron overload in prostate cancer cells.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- β2-microglobulin induced apoptosis of tumor cells via the ERK signaling pathway by directly interacting with HFE in HER2-overexpressing breast cancer.BMC cancer · 2024Article
- Ferroptosis landscape in prostate cancer from molecular and metabolic perspective.Cell death discovery · 2023Review
- HFE promotes mitotic cell division through recruitment of cytokinetic abscission machinery in hepatocellular carcinoma.Oncogene · 2022Article
- Impact of beta-2 microglobulin expression on the survival of glioma patients via modulating the tumor immune microenvironment.CNS neuroscience & therapeutics · 2021Article
- The Implication and Significance of Beta 2 Microglobulin: A Conservative Multifunctional Regulator.Chinese medical journal · 2016Review
- Iron homeostasis and tumorigenesis: molecular mechanisms and therapeutic opportunities.Protein & cell · 2015Review
- RANK-mediated signaling network and cancer metastasis.Cancer metastasis reviews · 2014Review
- miR-409-3p/-5p promotes tumorigenesis, epithelial-to-mesenchymal transition, and bone metastasis of human prostate cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Evidence for the Influence of the Iron Regulatory MHC Class I Molecule HFE on Tumor Progression in Experimental Models and Clinical Populations.Translational oncogenomics · 2014Review
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
Abstract
backgroundBone metastasis is the most lethal form of several cancers. The β2-microglobulin (β2-M)/hemochromatosis (HFE) complex plays an important role in cancer development and bone metastasis. We demonstrated previously that overexpression of β2-M in prostate, breast, lung and renal cancer leads to increased bone metastasis in mouse models. Therefore, we hypothesized that β2-M is a rational target to treat prostate cancer bone metastasis.
resultsIn this study, we demonstrate the role of β2-M and its binding partner, HFE, in modulating radiation sensitivity and chemo-sensitivity of prostate cancer. By genetic deletion of β2-M or HFE or using an anti-β2-M antibody (Ab), we demonstrate that prostate cancer cells are sensitive to radiation in vitro and in vivo. Inhibition of β2-M or HFE sensitized prostate cancer cells to radiation by increasing iron and reactive oxygen species and decreasing DNA repair and stress response proteins. Using xenograft mouse model, we demonstrate that anti-β2-M Ab sensitizes prostate cancer cells to radiation treatment. Additionally, anti-β2-M Ab was able to prevent tumor growth in an immunocompetent spontaneous prostate cancer mouse model. Since bone metastasis is lethal, we used a bone xenograft model to test the ability of anti-β2-M Ab and radiation to block tumor growth in the bone. Combination treatment significantly prevented tumor growth in the bone xenograft model by inhibiting β2-M and inducing iron overload. In addition to radiation sensitive effects, inhibition of β2-M sensitized prostate cancer cells to chemotherapeutic agents.
conclusionSince prostate cancer bone metastatic patients have high β2-M in the tumor tissue and in the secreted form, targeting β2-M with anti-β2-M Ab is a promising therapeutic agent. Additionally, inhibition of β2-M sensitizes cancer cells to clinically used therapies such as radiation by inducing iron overload and decreasing DNA repair enzymes.
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