ArticleOncogene2007
The tyrosine kinase Abl is required for Src-transforming activity in mouse fibroblasts and human breast cancer cells.
Article in Oncogene, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 63 citations in OpenAlex.
- Src and Abl as Therapeutic Targets in Lung Cancer: Opportunities for Drug Repurposing.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Styrylquinazoline derivatives as ABL inhibitors selective for different DFG orientations.Journal of enzyme inhibition and medicinal chemistry · 2023Article
- Article
- Targeting key transcriptional factor STAT3 in colorectal cancer.Molecular and cellular biochemistry · 2021Review
- EnABLing Tumor Growth and Progression: Recent progress in unraveling the functions of ABL kinases in solid tumor cells.Current pharmacology reports · 2018Article
- Advances in studies of tyrosine kinase inhibitors and their acquired resistance.Molecular cancer · 2018Review
- Atomic view of the energy landscape in the allosteric regulation of Abl kinase.Nature structural & molecular biology · 2017Article
- Targeting Aberrant p70S6K Activation for Estrogen Receptor-Negative Breast Cancer Prevention.Cancer prevention research (Philadelphia, Pa.) · 2017Article
- Mutant p53 dictates the oncogenic activity of c-Abl in triple-negative breast cancers.Cell death & disease · 2017Article
- Novel Src/Abl tyrosine kinase inhibitor bosutinib suppresses neuroblastoma growth via inhibiting Src/Abl signaling.Oncotarget · 2017Article
- c-Abl inhibits breast cancer tumorigenesis through reactivation of p53-mediated p21 expression.Oncotarget · 2016Article
- ABL kinases promote breast cancer osteolytic metastasis by modulating tumor-bone interactions through TAZ and STAT5 signaling.Science signaling · 2016Article
- Combined inhibition of EGFR and c-ABL suppresses the growth of triple-negative breast cancer growth through inhibition of HOTAIR.Oncotarget · 2015Article
- The proto-oncogene c-Src and its downstream signaling pathways are inhibited by the metastasis suppressor, NDRG1.Oncotarget · 2015Article
- ABL tyrosine kinase inhibition variable effects on the invasive properties of different triple negative breast cancer cell lines.PloS one · 2015Article
- Suppressor of cytokine signaling 1 modulates invasion and metastatic potential of colorectal cancer cells.Molecular oncology · 2014Article
- Clinical targeting of mutated and wild-type protein tyrosine kinases in cancer.Molecular and cellular biology · 2014Review
- Article
- Role of ABL family kinases in cancer: from leukaemia to solid tumours.Nature reviews. Cancer · 2013Review
- Analysis of SRC oncogenic signaling in colorectal cancer by stable isotope labeling with heavy amino acids in mouse xenografts.Molecular & cellular proteomics : MCP · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The cytoplasmic tyrosine kinase Src has been implicated in signal transduction induced by growth factors and integrins. Src also shows oncogenic activity when deregulated. Accumulating evidence indicates that the tyrosine kinase Abl is an important substrate for Src signalling in normal cells. Here we show that Abl is also required for Src-induced transformation of mouse fibroblasts. Abl does not mediate tyrosine phosphorylation of Stat3 and Shc, two important regulators of Src oncogenic activity. In contrast, Abl controls the activation of the small GTPase Rac for oncogenic signalling and active Rac partly rescued Src transformation in cells with inactive Abl. Moreover, Abl mediates Src-induced extracellular regulated kinase 5 (ERK5) activation to drive cell transformation. Finally, we find that Abl/Rac and Abl/ERK5 pathways also operate in human MCF7 and BT549 breast cancer cells, where neoplastic transformation depends on Src-like activities. Therefore, Abl is an important regulator of Src oncogenic activity both in mouse fibroblasts and in human cancer cells. Targeting these Abl-dependent signalling cascades may be of therapeutic value in breast cancers where Src-like function is important.
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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.