ArticleOncogene2001
Novel cross talk between MEK and S6K2 in FGF-2 induced proliferation of SCLC cells.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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
38 citing papers in PubMed, 73 citations in OpenAlex.
- S6K2 in Focus: Signaling Pathways, Post-Translational Modifications, and Computational Analysis.International journal of molecular sciences · 2024Review
- Targeted Therapies in Small Cell Lung Cancer: From Old Failures to Novel Therapeutic Strategies.International journal of molecular sciences · 2023Review
- Asymmetric Dimethylation of Ribosomal S6 Kinase 2 Regulates Its Cellular Localisation and Pro-Survival Function.International journal of molecular sciences · 2023Article
- Review
- Antitumor activity and mechanism of resistance of the novel HDAC and PI3K dual inhibitor CUDC-907 in pancreatic cancer.Cancer chemotherapy and pharmacology · 2021Article
- FGFR1 Is Critical for RBL2 Loss-Driven Tumor Development and Requires PLCG1 Activation for Continued Growth of Small Cell Lung Cancer.Cancer research · 2020Article
- FGFR1 Oncogenic Activation Reveals an Alternative Cell of Origin of SCLC in Rb1/p53 Mice.Cell reports · 2020Article
- Distinct Roles of mTOR Targets S6K1 and S6K2 in Breast Cancer.International journal of molecular sciences · 2020Review
- Locus Mapping, Molecular Cloning, and Expression Analysis of rps6kb2, a Novel Metamorphosis-Related Gene in Chinese Tongue Sole (Cynoglossus semilaevis).Marine biotechnology (New York, N.Y.) · 2017Article
- MicroRNA-Related Polymorphisms in PI3K/Akt/mTOR Pathway Genes Are Predictive of Limited-Disease Small Cell Lung Cancer Treatment Outcomes.BioMed research international · 2017Article
- Unique and Redundant Functions of p70 Ribosomal S6 Kinase Isoforms Regulate Mesenchymal Cell Proliferation and Migration in Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2016Article
- S6K2-mediated regulation of TRBP as a determinant of miRNA expression in human primary lymphatic endothelial cells.Nucleic acids research · 2016Article
- Is the Canonical RAF/MEK/ERK Signaling Pathway a Therapeutic Target in SCLC?Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2016Review
- mTor signaling is required for the formation of proliferating Müller glia-derived progenitor cells in the chick retina.Development (Cambridge, England) · 2016Article
- [Advances on Driver Mutations of Small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2016Review
- Nemo-like kinase regulates the expression of vascular endothelial growth factor (VEGF) in alveolar epithelial cells.Scientific reports · 2016Article
- Expression of phosphorylated mTOR and its clinical significances in small cell lung cancer.International journal of clinical and experimental pathology · 2015Article
- hnRNPA1 couples nuclear export and translation of specific mRNAs downstream of FGF-2/S6K2 signalling.Nucleic acids research · 2014Article
- PD173074, a selective FGFR inhibitor, reverses MRP7 (ABCC10)-mediated MDR.Acta pharmaceutica Sinica. B · 2014Article
- Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Here, we show that fibroblast growth factor-2 (FGF-2) induces proliferation of H-510 and H-69 small cell lung cancer (SCLC) cells. However, the optimal response to FGF-2 was obtained at 10-fold lower concentrations in H-510 cells. This correlated with the selective activation of the mitogen-activated protein kinase kinase (MEK) pathway in H-510, but not H-69 cells. Moreover, inhibition of MEK with PD098059 blocked FGF-2-induced proliferation in H-510 cells only. Similarly, ribosomal protein S6 kinase 2 (S6K2), a recently identified homologue of S6K1 was activated by FGF-2 in H-510, but not H-69 cells. This activation was independent of phosphatidylinositol-3 kinase, but was sensitive to inhibition of the MEK pathway. These data suggest that S6K2 is a novel downstream target of MEK. The potency of FGF-2 in H-510 cells might reflect this additional MEK/S6K2 signalling. In contrast to S6K2, S6K1 was activated in both SCLC cell lines. Inhibition of the mammalian target of rapamycin with 10 ng/ml rapamycin blocked S6K1 activation and proliferation of both lines. However, even at 100 ng/ml, rapamycin only partially inhibited S6K2. Strikingly, this correlated with inhibition of MEK signalling. Our data indicate that S6K1, and possibly S6K2, are involved in FGF-2-induced SCLC cell growth, a notion supported by the overexpression and higher baseline activity of both isoforms in SCLC lines, as compared to normal human type-II pneumocytes.
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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.