ArticleOncogene2009
LMO4 is an essential mediator of ErbB2/HER2/Neu-induced breast cancer cell cycle progression.
Article in Oncogene, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 48 citations in OpenAlex.
- Genome-wide association study in East Asians identifies two novel breast cancer susceptibility loci.Human molecular genetics · 2016Trial
- Targeting YES1 Disrupts Mitotic Fidelity and Potentiates the Response to Taxanes in Triple-Negative Breast Cancer.Cancer research · 2024Article
- LIN9 and NEK2 Are Core Regulators of Mitotic Fidelity That Can Be Therapeutically Targeted to Overcome Taxane Resistance.Cancer research · 2020Article
- LMO4 promotes the invasion and proliferation of gastric cancer by activating PI3K-Akt-mTOR signaling.American journal of translational research · 2019Article
- LMO1 functions as an oncogene by regulating TTK expression and correlates with neuroendocrine differentiation of lung cancer.Oncotarget · 2018Article
- iCopyDAV: Integrated platform for copy number variations-Detection, annotation and visualization.PloS one · 2018Article
- LMO4 mediates trastuzumab resistance in HER2 positive breast cancer cells.American journal of cancer research · 2018Article
- Genetic susceptibility to neuroblastoma.Current opinion in genetics & development · 2017Review
- Bromodomain and Extraterminal Protein Inhibition Blocks Growth of Triple-negative Breast Cancers through the Suppression of Aurora Kinases.The Journal of biological chemistry · 2016Article
- The LMO2 oncogene regulates DNA replication in hematopoietic cells.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Article
- Anxious moments for the protein tyrosine phosphatase PTP1B.Trends in neurosciences · 2015Article
- The co-factor of LIM domains (CLIM/LDB/NLI) maintains basal mammary epithelial stem cells and promotes breast tumorigenesis.PLoS genetics · 2014Article
- LIM-domain-only proteins: multifunctional nuclear transcription coregulators that interacts with diverse proteins.Molecular biology reports · 2014Review
- Article
- The oncoprotein HBXIP activates transcriptional coregulatory protein LMO4 via Sp1 to promote proliferation of breast cancer cells.Carcinogenesis · 2013Article
- LIM-domain-only proteins in cancer.Nature reviews. Cancer · 2013Review
- Identification of PADI2 as a potential breast cancer biomarker and therapeutic target.BMC cancer · 2012Article
- β-cell-specific gene repression: a mechanism to protect against inappropriate or maladjusted insulin secretion?Diabetes · 2012Article
- Novel amplifications in pediatric medulloblastoma identified by genome-wide copy number profiling.Journal of neuro-oncology · 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
6 authors at 3 institutions in 2 countries.
Funding
Abstract
ErbB2/HER2/Neu-overexpressing breast cancers are characterized by poor survival due to high proliferation and metastasis rates and identifying downstream targets of ErbB2 should facilitate developing novel therapies for this disease. Gene expression profiling revealed the transcriptional regulator LIM-only protein 4 (LMO4) is upregulated during ErbB2-induced mouse mammary gland tumorigenesis. Although LMO4 is frequently overexpressed in breast cancer and LMO4-overexpressing mice develop mammary epithelial tumors, the mechanisms involved are unknown. In this study, we report that LMO4 is a downstream target of ErbB2 and PI3K in ErbB2-dependent breast cancer cells. Furthermore, LMO4 silencing reduces proliferation of these cells, inducing a G2/M arrest that was associated with decreased cullin-3, an E3-ubiquitin ligase component important for mitosis. Loss of LMO4 subsequently results in reduced Cyclin D1 and Cyclin E. Further supporting a role for LMO4 in modulating proliferation by regulating cullin-3 expression, we found that LMO4 expression oscillates throughout the cell cycle with maximum expression occurring during G2/M and these changes precede oscillations in cullin-3 levels. LMO4 levels are also highest in high-grade/less differentiated breast cancers, which are characteristically highly proliferative. We conclude that LMO4 is a novel cell cycle regulator with a key role in mediating ErbB2-induced proliferation, a hallmark of ErbB2-positive disease.
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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.