ArticleOncogene2003
Naturally occurring dominant-negative Stat5 suppresses transcriptional activity of estrogen receptors and induces apoptosis in T47D breast cancer cells.
Article in Oncogene, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 81 citations in OpenAlex.
- A novel EGFR variant EGFRx maintains glioblastoma stem cells through STAT5.Neuro-oncology · 2024Article
- STAT family of transcription factors in breast cancer: Pathogenesis and therapeutic opportunities and challenges.Seminars in cancer biology · 2022Review
- STAT5b: A master regulator of key biological pathways.Frontiers in immunology · 2022Review
- Serine residues 726 and 780 have nonredundant roles regulating STAT5a activity in luminal breast cancer.Scientific reports · 2021Article
- Transcriptional down-regulation ofeLife · 2019Article
- Drosophila Jak/STAT Signaling: Regulation and Relevance in Human Cancer and Metastasis.International journal of molecular sciences · 2018Review
- Rare Variants in theDrug metabolism and disposition: the biological fate of chemicals · 2018Article
- 17Journal of the Endocrine Society · 2018Article
- Article
- Regulation of transcriptional activation function of rat estrogen receptor α (ERα) by novel C-terminal splice inserts.Molecular and cellular endocrinology · 2015Article
- miR-221/222 control luminal breast cancer tumor progression by regulating different targets.Cell cycle (Georgetown, Tex.) · 2014Article
- [Mechanisms of EGF regulation of COX-2 through the STAT5 signaling pathway in human lung adenocarcinoma A549 cells].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2013Article
- Nucleic acid-based approaches to STAT inhibition.JAK-STAT · 2012Review
- Robust identification of transcriptional regulatory networks using a Gibbs sampler on outlier sum statistic.Bioinformatics (Oxford, England) · 2012Article
- Involvement of ER-α36, Src, EGFR and STAT5 in the biphasic estrogen signaling of ER-negative breast cancer cells.Oncology reports · 2012Article
- Article
- Estrogen receptor-alpha 36 mediates mitogenic antiestrogen signaling in ER-negative breast cancer cells.PloS one · 2012Article
- Coffee polyphenols change the expression of STAT5B and ATF-2 modifying cyclin D1 levels in cancer cells.Oxidative medicine and cellular longevity · 2012Article
- A switch role of Src in the biphasic EGF signaling of ER-negative breast cancer cells.PloS one · 2012Article
- GH modulates hepatic epidermal growth factor signaling in the mouse.The Journal of endocrinology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signal transducer and activator of transcription (Stat) 5 regulates growth, differentiation, and survival of mammary and hematopoietic cells. The role of Stat5 in breast cancer has not been established, although Stat5 is critical for some hematopoietic malignancies. We detected for the first time that Stat5b is constitutively activated in human breast cancer cell lines, and analysed the role of Stat5 in estrogen receptor(ER)-positive breast cancer cell lines using dominant-negative variants of Stat5. Two distinct carboxyl-truncated Stat5a derivatives were generated. Stat5aDelta740 corresponded to a naturally occurring alternative splice variant, and Stat5aDelta713 was analogous to an 80 kDa Stat5a product of a nuclear protease. Stat5aDelta740 and Stat5aDelta713 displayed comparable dominant-negative properties and suppressed transcriptional activity of wild-type Stat5a and Stat5b equally well. Cotransfection experiments revealed that Stat5aDelta740 completely blocked transcriptional activity of endogenous estrogen receptor in T47D and MCF7 cells, and of both ER alpha and ER beta in COS-7 cells. Stat5aDelta740 was selected for adenoviral delivery, and high-efficiency expression of tyrosine phosphorylated Stat5aDelta740 was achieved in infected cells. Adenoviral-mediated Stat5aDelta740 induced apoptosis in T47D cells but not in caspase-3-negative MCF7 cells. The present study indicates that overexpression of a dominant-negative variant of Stat5 suppresses ER transcriptional activity and induces apoptosis in estrogen-responsive breast cancer tissue culture cells.
Indexed as
Identifiers
What OpenQuestion holds
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.