ArticleOncogene2003
An inhibitory function for JNK in the regulation of IGF-I signaling in breast cancer.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
The trial behind it
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
16 citing papers in PubMed, 45 citations in OpenAlex.
- Losartan rewires the tumor-immune microenvironment and suppresses IGF-1 to overcome resistance to chemo-immunotherapy in ovarian cancer.British journal of cancer · 2024Article
- Global signalling network analysis of luminal T47D breast cancer cells in response to progesterone.Frontiers in endocrinology · 2022Article
- Conflicting evidence for the role of JNK as a target in breast cancer cell proliferation: Comparisons between pharmacological inhibition and selective shRNA knockdown approaches.Pharmacology research & perspectives · 2018Article
- A c-Jun N-terminal kinase inhibitor, JNK-IN-8, sensitizes triple negative breast cancer cells to lapatinib.Oncotarget · 2017Article
- Clinicopathological and prognostic significance of mitogen-activated protein kinases (MAPK) in breast cancers.Breast cancer research and treatment · 2016Article
- Insulin-like growth factor and epidermal growth factor signaling in breast cancer cell growth: focus on endocrine resistant disease.Analytical cellular pathology (Amsterdam) · 2015Review
- JNK signalling in cancer: in need of new, smarter therapeutic targets.British journal of pharmacology · 2014Review
- Promoting longevity by maintaining metabolic and proliferative homeostasis.The Journal of experimental biology · 2014Review
- p53 is a key regulator for osthole-triggered cancer pathogenesis.BioMed research international · 2014Article
- Misregulation of an adaptive metabolic response contributes to the age-related disruption of lipid homeostasis in Drosophila.Cell reports · 2013Article
- Association of a common genetic variant of the IGF-1 gene with event-free survival in patients with HER2-positive breast cancer.Journal of cancer research and clinical oncology · 2013Article
- α-TEA cooperates with MEK or mTOR inhibitors to induce apoptosis via targeting IRS/PI3K pathways.British journal of cancer · 2011Article
- c-Jun N-terminal Kinase 2 Regulates Multiple Receptor Tyrosine Kinase Pathways in Mouse Mammary Tumor Growth and Metastasis.Genes & cancer · 2011Article
- Insulin and JNK: optimizing metabolic homeostasis and lifespan.Trends in endocrinology and metabolism: TEM · 2009Review
- IGF and insulin receptor signaling in breast cancer.Journal of mammary gland biology and neoplasia · 2008Article
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Insulin-like growth factor-I receptor (IGF-IR) is frequently overexpressed in a variety of cancer types. Since many breast tumors and cancer cell lines overexpress IGF-IR, we tested IGF-I effects on chemotherapy-treated breast cancer cells. IGF-I protects from chemotherapy-induced apoptosis, suggesting that overlapping signaling pathways modulate IGF-I and chemotherapy treatment outcomes. Taxol and other chemotherapy drugs induce c-Jun N-terminal kinase (JNK), a kinase that conveys cellular stress and death signals. Notably, in this paper we show that IGF-I alone induces a potent JNK response and this activity is reversed by inhibition of phosphatidylinositol 3-kinase (PI 3-kinase) with LY294002 in MCF-7 but not T47D cells. Cotreatment of cells with chemotherapy and IGF-I leads to additive JNK responses. Using cells overexpressing Akt, we confirm that IGF-I-mediated survival is Akt dependent. In contrast, overexpression of JNK significantly enhances Taxol-induced apoptosis and inhibits IGF-I survival effects. Further, JNK attenuates anchorage-independent growth of MCF-7 cells. The inhibitory effect of JNK appears to be mediated by serine phosphorylation of IRS-1 (insulin receptor substrate) since both Taxol and IGF-I treatment enhanced Ser(312) IRS-1 phosphorylation, while LY294002 blocked IGF-I-mediated phosphorylation. Taken together, these data provide a mechanism whereby stress or growth factors activate JNK to reduce proliferation and/or survival in breast cancer cells.
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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 Socratic graph.