ArticleThe Journal of biological chemistry2009
Selective activation of trophoblast-specific PLAC1 in breast cancer by CCAAT/enhancer-binding protein beta (C/EBPbeta) isoform 2.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 31 citations in OpenAlex.
- CEBPB emerges as a key regulatory factor in human cancers through diverse molecular mechanisms and clinical implications.Discover oncology · 2025Review
- The Synthetic Curcumin Analog HO-3867 Rescues Suppression of PLAC1 Expression in Ovarian Cancer Cells.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Placenta-specific protein 1 enhances liver metastatic potential and is associated with the PI3K/AKT/NF-κB signaling pathway in colorectal cancer.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2021Article
- Analysis of core genes for colorectal cancer prognosis based on immune and stromal scores.PeerJ · 2021Article
- PLAC1 is essential for FGF7/FGFRIIIb-induced Akt-mediated cancer cell proliferation.Oncotarget · 2020Article
- Involvement of the Endocrine-Disrupting Chemical Bisphenol A (BPA) in Human Placentation.Journal of clinical medicine · 2020Article
- PLAC1: biology and potential application in cancer immunotherapy.Cancer immunology, immunotherapy : CII · 2019Review
- Plac1 Is a Key Regulator of the Inflammatory Response and Immune Tolerance In Mammary Tumorigenesis.Scientific reports · 2018Article
- PLAC1-specific TCR-engineered T cells mediate antigen-specific antitumor effects in breast cancer.Oncology letters · 2018Article
- Placenta-specific protein 1 promotes cell proliferation and invasion in non-small cell lung cancer.Oncology reports · 2018Article
- PLAC1 as a serum biomarker for breast cancer.PloS one · 2018Article
- Placenta-specific protein 1: a potential key to many oncofetal-placental OB/GYN research questions.Obstetrics and gynecology international · 2014Article
- NCOA3 is a selective co-activator of estrogen receptor α-mediated transactivation of PLAC1 in MCF-7 breast cancer cells.BMC cancer · 2013Article
- PPARδ induces estrogen receptor-positive mammary neoplasia through an inflammatory and metabolic phenotype linked to mTOR activation.Cancer research · 2013Article
- The oncoplacental gene placenta-specific protein 1 is highly expressed in endometrial tumors and cell lines.Obstetrics and gynecology international · 2013Article
- RXRα and LXR activate two promoters in placenta- and tumor-specific expression of PLAC1.Placenta · 2011Article
- Progesterone induces expression of the prolactin receptor gene through cooperative action of Sp1 and C/EBP.Molecular and cellular endocrinology · 2011Article
- Tumor-associated CpG demethylation augments hypoxia-induced effects by positive autoregulation of HIF-1α.Oncogene · 2011Article
- Article
- C/EBPβ's role in determining Ras-induced senescence or transformation.Small GTPases · 2011Article
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
No grant is acknowledged in the PubMed record.
Abstract
The trophoblast-specific gene PLAC1 (placenta-specific 1) is ectopically expressed in a wide range of human malignancies, most frequently in breast cancer, and is essentially involved in cancer cell proliferation, migration, and invasion. Here we show that basal activity of the PLAC1 promoter is selectively controlled by ubiquitous transcription factor SP1 and isoform 2 of CCAAT/enhancer-binding protein beta that we found to be selectively expressed in placental tissue and cancer cells. Binding of both factors to their respective elements within the PLAC1 promoter was essential to attain full promoter activity. Estrogen receptor alpha (ERalpha) signaling further augmented transcription and translation of PLAC1 and most likely accounts for the positive correlation between PLAC1 expression levels and the ERalpha status we observed in primary breast cancer specimens. DNA affinity precipitation and chromatin immunoprecipitation assays revealed that transactivation of the PLAC1 promoter by ligand-activated ERalpha is based on a nonclassical pathway independent of estrogen-response elements, by tethering of ERalpha to DNA-bound CCAAT/enhancer-binding protein beta-2, and SP1. Our findings provide first insight into a novel and hitherto unknown regulatory mechanism governing selective activation of trophoblast-specific gene expression in breast cancer.
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.