ArticleCancer letters2014
Osteopontin-a alters glucose homeostasis in anchorage-independent breast cancer cells.
Article in Cancer letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 30 citations in OpenAlex.
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- Cancer metastasis: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2025Review
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- Feed-forward loops between metastatic cancer cells and their microenvironment-the stage of escalation.EMBO molecular medicine · 2022Review
- Metabolic profiling of attached and detached metformin and 2-deoxy-D-glucose treated breast cancer cells reveals adaptive changes in metabolome of detached cells.Scientific reports · 2021Article
- Evaluating line-broadening factors on a reference spectrum as a bucketing method for NMR based metabolomics.Analytical biochemistry · 2020Article
- Bone Tropism in Cancer Metastases.Cold Spring Harbor perspectives in medicine · 2020Review
- Metastasis Organotropism: Redefining the Congenial Soil.Developmental cell · 2019Review
- Unique Metabolic Adaptations Dictate Distal Organ-Specific Metastatic Colonization.Cancer cell · 2018Review
- Systematic analysis of genes involved in oral cancer metastasis to lymph nodes.Cellular & molecular biology letters · 2018Article
- A core program of gene expression characterizes cancer metastases.Oncotarget · 2017Article
- Activation of carbonic anhydrase IX by alternatively spliced tissue factor under late-stage tumor conditions.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- OPN-a induces muscle inflammation by increasing recruitment and activation of pro-inflammatory macrophages.Experimental physiology · 2016Article
- Osteopontin-a splice variant is overexpressed in papillary thyroid carcinoma and modulates invasive behavior.Oncotarget · 2016Article
- Time and Circumstances: Cancer Cell Metabolism at Various Stages of Disease Progression.Frontiers in oncology · 2016Review
- Role of osteopontin in the pathophysiology of cancer.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Invasive breast tumor cells generate three splice variants of the metastasis gene osteopontin, while non-invasive breast cells express only the unspliced form or no osteopontin at all. One role for osteopontin in tumor progression is the support of anchorage-independence. Here we show that the full-length gene product, osteopontin-a, induces a gene expression profile that is associated with tissue remodeling and directed movement/sprouting. This occurs via signals through STAT1 and STAT3 to sn-glycero-3-phosphocholine. Osteopontin-a upregulates the levels of glucose in breast cancer cells, likely through STAT3 and its transcriptional targets apolipoprotein D and IGFBP5. The splice variants osteopontin-a and osteopontin-c may synergize, with each form activating signal transduction pathways that are distinct from the other. The elevated glucose is used by osteopontin-c dependent signals to generate chemical energy (Shi et al. submitted for publication). The splice variant-specific metabolic effects of osteopontin add a novel aspect to the pro-metastatic functions of this molecule.
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Registered trials
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