ArticleCancer research2010
Prolactin inhibits BCL6 expression in breast cancer through a Stat5a-dependent mechanism.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 79 citations in OpenAlex.
- In-silico Exploration of the Possible Prolactin Pathway Related Targets of B. Monnieri against Triple Negative Breast Cancer: Selection of the Best Target Ligand Combination.Cell biochemistry and biophysics · 2026Article
- STAT-independent functions of Janus kinases 1 and 2 are obligatory for the postnatal development of mammary epithelial ducts.Cell reports · 2026Article
- The Roles of STAT3 and STAT5 in Breast Cancer.Cancers · 2025Review
- Review
- Notch3 restricts metastasis of breast cancers through regulation of the JAK/STAT5A signaling pathway.BMC cancer · 2023Article
- BTB protein family and human breast cancer: signaling pathways and clinical progress.Journal of cancer research and clinical oncology · 2023Review
- Loss of Epigenetic Regulation Disrupts Lineage Integrity, Induces Aberrant Alveogenesis, and Promotes Breast Cancer.Cancer discovery · 2022Article
- Breast Cancer and Prolactin - New Mechanisms and Models.Endocrinology · 2022Review
- Article
- Prolactin: The Third Hormone in Breast Cancer.Frontiers in endocrinology · 2022Review
- Terminal differentiation and anti-tumorigenic effects of prolactin in breast cancer.Frontiers in endocrinology · 2022Review
- Review
- An in vivo genome-wide shRNA screen identifies BCL6 as a targetable biomarker of paclitaxel resistance in breast cancer.Molecular oncology · 2021Article
- Disruption of STAT5A and NMI signaling axis leads to ISG20-driven metastatic mammary tumors.Oncogenesis · 2021Article
- A Framework of All Discovered Immunological Pathways and Their Roles for Four Specific Types of Pathogens and Hypersensitivities.Frontiers in immunology · 2020Review
- Drosophila Jak/STAT Signaling: Regulation and Relevance in Human Cancer and Metastasis.International journal of molecular sciences · 2018Review
- Implications of STAT3 and STAT5 signaling on gene regulation and chromatin remodeling in hematopoietic cancer.Leukemia · 2018Review
- Knockdown of BCL6 Inhibited Malignant Phenotype and Enhanced Sensitivity of Glioblastoma Cells to TMZ through AKT Pathway.BioMed research international · 2018Article
- Apoptosis in inner ear sensory hair cells.Journal of otology · 2017Review
- BCL6 mRNA Expression Level in Invasive Duct Carcinoma not otherwise Specified.Journal of clinical and diagnostic research : JCDR · 2016Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
BCL6 is a transcriptional repressor that recognizes DNA target sequences similar to those recognized by signal transducer and activator of transcriptions 5 (Stat5). BCL6 disrupts differentiation of breast epithelia, is downregulated during lactation, and is upregulated in poorly differentiated breast cancer. In contrast, Stat5a mediates prolactin-induced differentiation of mammary epithelia, and loss of Stat5 signaling in human breast cancer is associated with undifferentiated histology and poor prognosis. Here, we identify the mammary cell growth factor prolactin as a potent suppressor of BCL6 protein expression in human breast cancer through a mechanism that requires Stat5a, but not prolactin-activated Stat5b, MEK-ERK, or PI3K-AKT pathways. Prolactin rapidly suppressed BCL6 mRNA in T47D, MCF7, ZR75.1, and SKBr3 breast cancer cell lines, followed by prolonged reduction of BCL6 protein levels within 3 hours. Prolactin suppression of BCL6 was enhanced by overexpression of Stat5a but not Stat5b, was mimicked by constitutively active Stat5a, but did not require the transactivation domain of Stat5a. Stat5 chromatin immunoprecipitation demonstrated physical interaction with a BCL6 gene regulatory region, and BCL6 transcript repression required histone deacetylase activity based on sensitivity to trichostatin A. Functionally, BCL6 overexpression disrupted prolactin induction of Stat5 reporter genes. Prolactin suppression of BCL6 was extended to xenotransplant tumors in nude mice in vivo and to freshly isolated human breast cancer explants ex vivo. Quantitative immunohistochemistry revealed elevated BCL6 in high-grade and metastatic breast cancer compared with ductal carcinoma in situ and nonmalignant breast, and cellular BCL6 protein levels correlated negatively with nuclear Stat5a (r = -0.52; P < 0.001) but not with Stat5b. Loss of prolactin-Stat5a signaling and concomitant upregulation of BCL6 may represent a regulatory switch facilitating undifferentiated histology and poor prognosis of breast cancer.
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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.