ArticleJournal of molecular biology2013
Serum deprivation confers the MDA-MB-231 breast cancer line with an EGFR/JAK3/PLD2 system that maximizes cancer cell invasion.
Article in Journal of molecular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Functional requirements of the liver isoform of phosphofructokinase-1 in breast cancer cell migration.Journal of cell science · 2025Article
- An analytical screening platform to differentiate acute and prolonged exposures of per- and polyfluoroalkyl substances on invasive cellular phenotypes.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
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- JAK3/STAT5 signaling-triggered upregulation of PIK3CD contributes to gastric carcinoma development.Journal of cell communication and signaling · 2024Article
- Triple Negative Breast Cancer Preclinical Therapeutic Management by a Cationic Ruthenium-Based Nucleolipid Nanosystem.International journal of molecular sciences · 2023Article
- Effects and Mechanisms of Action of Preussin, a Marine Fungal Metabolite, against the Triple-Negative Breast Cancer Cell Line, MDA-MB-231, in 2D and 3D Cultures.Marine drugs · 2023Article
- Aldolase A and Phospholipase D1 Synergistically Resist Alkylating Agents and Radiation in Lung Cancer.Frontiers in oncology · 2021Article
- Profilin: many facets of a small protein.Biophysical reviews · 2020Review
- A Targeted Quantitative Proteomic Method Revealed a Substantial Reprogramming of Kinome during Melanoma Metastasis.Scientific reports · 2020Article
- High Expression of PhospholipaseD2 Induced by Hypoxia Promotes Proliferation of Colon Cancer Cells through Activating NF- κ Bp65 Signaling Pathway.Pathology oncology research : POR · 2020Article
- Preparation and Evaluation of Liposomes Co-Loaded with Doxorubicin, Phospholipase D Inhibitor 5-Fluoro-2-Indolyl Deschlorohalopemide (FIPI) and D-Alpha Tocopheryl Acid Succinate (α-TOS) for Anti-Metastasis.Nanoscale research letters · 2019Article
- Emerging roles of lipid metabolism in cancer metastasis.Molecular cancer · 2017Review
- EGFR expression is associated with cytoplasmic staining of CXCR4 and predicts poor prognosis in triple-negative breast carcinomas.Oncology letters · 2017Article
- The Interaction between Cancer Stem Cell Marker CD133 and Src Protein Promotes Focal Adhesion Kinase (FAK) Phosphorylation and Cell Migration.The Journal of biological chemistry · 2016Article
- A Repertoire of MicroRNAs Regulates Cancer Cell Starvation by Targeting Phospholipase D in a Feedback Loop That Operates Maximally in Cancer Cells.Molecular and cellular biology · 2016Article
- Phosphatidic Acid (PA) can Displace PPARα/LXRα Binding to The EGFR Promoter Causing its Transrepression in Luminal Cancer Cells.Scientific reports · 2015Article
- Modulation of tumor fatty acids, through overexpression or loss of thyroid hormone responsive protein spot 14 is associated with altered growth and metastasis.Breast cancer research : BCR · 2014Article
- Phospholipase D in cell signaling: from a myriad of cell functions to cancer growth and metastasis.The Journal of biological chemistry · 2014Review
- Cellular heterogeneity profiling by hyaluronan probes reveals an invasive but slow-growing breast tumor subset.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Our laboratory has reported earlier that in leukocytes, phospholipase D2 (PLD2) is under control of Janus kinase 3 (JAK3), which mediates chemotaxis. Investigating JAK3 in cancer cells led to an important discovery as exponentially growing MDA-MB-231 human breast cancer cells, which are highly proliferative and metastatic, did not substantially use JAK3 to activate PLD2. However, in 2-h or 16-h starved cell cultures, JAK3 switches to a PLD2-enhancing role, consistent with the needs of those cells to enter a "survival state" that relies on an increase in PLD2 activity to withstand serum deprivation. Using a small-molecule tyrosine kinase inhibitor, the flavonoid 4',5,7-trihydroxyflavone (apigenin), as well as RNA silencing, we found that the invasive phenotype of MDA-MB-231 cells is mediated by PLD2 under direct regulation of both JAK3 and the tyrosine kinase, epidermal growth factor receptor (EGFR). Furthermore, serum-deprived cells in culture show an upregulated EGFR/JAK3/PLD2-PA system and are especially sensitive to a combination of JAK3 and PLD2 enzymatic activity inhibitors (30nM apigenin and 300nM 5-fluoro-2-indolyl des-chlorohalopemide (FIPI), respectively). Thus, a multi-layered activation of cell invasion by two kinases (EGFR and JAK3) and a phospholipase (PLD2) provides regulatory flexibility and maximizes the aggressively invasive power of MDA-MB-231 breast cancer cells. This is especially important in the absence of growth factors in serum, coincidental with migration of these cells to new locations.
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Registered trials
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.