ArticleOncogene2013
Peroxiredoxin 2 specifically regulates the oxidative and metabolic stress response of human metastatic breast cancer cells in lungs.
Article in Oncogene, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 71 papers.
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Who cites it
71 citing papers in PubMed, 105 citations in OpenAlex.
- Article
- Metabolic adaptations in cancer progression.Physiological reviews · 2026Review
- Spatiotemporal Heterogeneity of Tumor Glucose Metabolism Reprogramming: From Single-Cell Mechanisms to Precision Interventions.International journal of molecular sciences · 2025Review
- Development of a cuproptosis-related prognostic signature to reveal heterogeneity of the immune microenvironment and drug sensitivity in acute lymphoblastic leukemia.European journal of medical research · 2025Article
- Lung-specific metastasis: the coevolution of tumor cells and lung microenvironment.Molecular cancer · 2025Review
- Cancer metastasis: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2025Review
- Review
- GSTP1, PRDX2 and NFE2L2: Potential Markers for Primary Stage Breast Cancer.Current drug targets · 2025Article
- SOX11/PRDX2 axis modulates redox homeostasis and chemoresistance in aggressive mantle cell lymphoma.Scientific reports · 2024Article
- Metabolic heterogeneity in cancer.Nature metabolism · 2024Review
- Apolipoprotein E-depletion accelerates arterial fat deposition in the spontaneously hypertensive rat.Experimental animals · 2023Article
- Study on the Relationship Between Differentially Expressed Proteins in Breast Cancer and Lymph Node Metastasis.Advances in therapy · 2023Article
- Metabolic factors associated with the prognosis of oligometastatic patients treated with stereotactic body radiotherapy.Cancer metastasis reviews · 2023Review
- Stanniocalcin 1 promotes lung metastasis of breast cancer by enhancing EGFR-ERK-S100A4 signaling.Cell death & disease · 2023Article
- Breast cancer cells that preferentially metastasize to lung or bone are more glycolytic, synthesize serine at greater rates, and consume less ATP and NADPH than parent MDA-MB-231 cells.Cancer & metabolism · 2023Article
- An Overview: The Diversified Role of Mitochondria in Cancer Metabolism.International journal of biological sciences · 2023Review
- Mitochondrial Redox Metabolism: The Epicenter of Metabolism during Cancer Progression.Antioxidants (Basel, Switzerland) · 2021Review
- Dynamic Landscape of Extracellular Vesicle-Associated Proteins Is Related to Treatment Response of Patients with Metastatic Breast Cancer.Membranes · 2021Article
- Proteome profiling of human placenta reveals developmental stage-dependent alterations in protein signature.Clinical proteomics · 2021Article
- The metabolic adaptation mechanism of metastatic organotropism.Experimental hematology & oncology · 2021Review
11 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedDmitri, P [corrected to Petrov, D]
Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Little is known about metastatic pathways that are specific to the lung rather than other organs. We previously showed that antioxidant proteins such as peroxiredoxins were specifically upregulated in lung metastatic breast cancer cells. We hypothesize that cancer cells that live under aerobic conditions, as might be the case in lungs, protect themselves against the damage caused by reactive oxygen species (ROS). To examine this hypothesis, we studied the role of peroxiredoxin-2 (PRDX2) in lung vs bone metastasis formation. A metastatic variant of MDA-MB-435 breast cancer cells that specifically metastasize to lungs (435-L3) was transduced with short hairpin RNAs to specifically silence PRDX2. Conversely, a bone metastatic variant of MDA-MB-231 cells (BO2) was stably transfected to overexpress PRDX2. The 435-L3 cells silenced for PRDX2 were significantly more sensitive to H(2)O(2)-induced oxidative stress than the parental and scrambled transfected cells. BO2/PRDX2 cells produced less ROS than BO2/green fluorescent protein control cells under oxidative stress. Moreover, PRDX2 knockdown inhibited the growth of 435-L3 cells in the lungs, whereas lymph node metastasis remained unaffected. In contrast, PRDX2 overexpression in bone metastatic BO2 breast cancer cells led to drastic inhibition of the skeletal tumor burden and reduction of bone destruction. Furthermore, PRDX2 expression in breast cancer cells was associated with a glucose-dependent phenotype, different from bone metastatic cells. Overall, our results strongly suggest that PRDX2 is a targetable 'metabolic adaptor' driver protein implicated in the selective growth of metastatic cells in the lungs by protecting them against oxidative stress.
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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 OpenQuestion graph.