ArticleMolecular and cellular biology2003
Growth factor signaling induces metastasis genes in transformed cells: molecular connection between Akt kinase and osteopontin in breast cancer.
Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 66 citations in OpenAlex.
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- Alterations of Ion Homeostasis in Cancer Metastasis: Implications for Treatment.Frontiers in oncology · 2021Review
- Gene expression signatures of site-specificity in cancer metastases.Clinical & experimental metastasis · 2020Article
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- Synergistic Targeting HER2 and EGFR with Bivalent Aptamer-siRNA Chimera Efficiently Inhibits HER2-Positive Tumor Growth.Molecular pharmaceutics · 2018Article
- Inferring Intracellular Signal Transduction Circuitry from Molecular Perturbation Experiments.Bulletin of mathematical biology · 2018Article
- 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
- Kaempferol inhibits the production of ROS to modulate OPN-αvβ3 integrin pathway in HUVECs.Journal of physiology and biochemistry · 2016Article
- Role of osteopontin in the pathophysiology of cancer.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
- The inhibitory effects of extracellular ATP on the growth of nasopharyngeal carcinoma cells via P2Y2 receptor and osteopontin.Journal of experimental & clinical cancer research : CR · 2014Article
- Biomimetic tumor microenvironment on a microfluidic platform.Biomicrofluidics · 2013Review
- EGFR expression is linked to osteopontin and Nf-κB signaling in clear cell renal cell carcinoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2013Article
- Photoacoustic imaging: a potential tool to detect early indicators of metastasis.Expert review of medical devices · 2013Review
- Loss of tumor suppressor Merlin in advanced breast cancer is due to post-translational regulation.The Journal of biological chemistry · 2011Article
- Immunohistochemical detection of phospho-Akt, phospho-BAD, HER2 and oestrogen receptors alpha and beta in Malaysian breast cancer patients.Pathology oncology research : POR · 2010Article
- Epidermal growth factor induces HCCR expression via PI3K/Akt/mTOR signaling in PANC-1 pancreatic cancer cells.BMC cancer · 2010Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Malignant tumors are characterized by excessive growth, immortalization, and metastatic spread, whereas benign tumors do not express gene products that mediate invasion. The molecular basis for this difference is incompletely understood. We have screened signal transduction molecules associated with the epidermal growth factor (EGF) receptor and have identified constitutive phosphorylation, indicative of activation, of Akt kinase in MT2994 breast cancer cells. In contrast, cells of the benign breast epithelial cell lines Comma-D and FSK-7 are immortalized through pathways that are independent of the EGF-phosphatidylinositol 3-kinase-Akt kinase cascade, but this is not associated with invasiveness. Transfection of constitutively active Akt kinase causes accelerated cell division and osteopontin expression. Conversely, dominant-negative Akt kinase slows cell cycle progression and suppresses osteopontin expression. The manipulation of osteopontin expression in this setting by transfection of the gene or its antisense does not affect the growth rate of the cells but alters cell motility and anchorage independence. Therefore, Akt kinase activates two distinct genetic programs: the program of growth and survival, which is independent of osteopontin expression, and the program of invasiveness and anchorage independence, which is mediated by osteopontin. These studies define Akt kinase as a molecular bridge between cell cycle progression and dissemination.
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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.