ArticleExperimental and therapeutic medicine2017
CCAAT enhancer binding protein β has a crucial role in regulating breast cancer cell growth via activating the TGF-β-Smad3 signaling pathway.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- CEBPB emerges as a key regulatory factor in human cancers through diverse molecular mechanisms and clinical implications.Discover oncology · 2025Review
- Drug Resistance Analysis of Pancreatic Cancer Based on Universally Differentially Expressed Genes.International journal of molecular sciences · 2025Article
- Association between PDCD6-VNTR polymorphism and urinary cancer susceptibility.Genes & genomics · 2024Article
- Multidimensional outlook on the pathophysiology of cervical cancer invasion and metastasis.Molecular and cellular biochemistry · 2023Review
- Review
- The roles of protocadherin-7 in colorectal cancer cells on cell proliferation and its chemoresistance.Frontiers in pharmacology · 2023Article
- VNTR polymorphism in the breakpoint region of ABL1 and susceptibility to bladder cancer.BMC medical genomics · 2021Article
- The Clinical Significance and Biological Function ofCancer management and research · 2021Article
- Dominant-Negative ATF5 Compromises Cancer Cell Survival by Targeting CEBPB and CEBPD.Molecular cancer research : MCR · 2020Article
- C/EBPβ and YY1 bind and interact with Smad3 to modulate lipopolysaccharide-induced amelotin gene transcription in mouse gingival epithelial cells.FEBS open bio · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to examine the effect of CCAAT enhancer binding protein β (C/EBPβ) on human breast cancer cells. The plasmids pCDH-C/EBPβ and pLKO.1-shC/EBPβ were constructed and were infected into MDA-MB-468 cells, to provide C/EBPβ overexpressing and C/EBPβ knockdown cells, respectively. Cell viability, cell cycle and apoptosis were observed by MTT assay and flow cytometry analysis. Protein expression levels of C/EBPβ, TGF-β1, P-Smad3 and Smad3 were detected by western blotting. MTT assay showed that the absorbance of MDA-MB-468 cells in the pCDH-C/EBPβ group was increased, whereas that in the pLKO.1-shC/EBPβ group was decreased, compared with the respective control at 48 and 72 h. Flow cytometric analysis indicated that the percentage of cells in the G2 phase was significantly increased in the pCDH-C/EBPβ group (P<0.05) and decreased in the pLKO.1-shC/EBPβ group compared with the respective control group. The proportion of apoptotic cells was decreased in the pCDH-C/EBPβ group and increased in the pLKO.1-shC/EBPβ group compared with the controls. The scratch-wound assay revealed that MDA-MB-468 cells depleted of C/EBPβ exhibited reduced motility compared with the control cells. Moreover, western blotting demonstrated that pCDH-C/EBPβ increased transforming growth factor (TGF)β1 and P-Smad3 protein expression and decreased Smad3 protein expression, whereas pLKO.1-shC/EBPβ decreased TGFβ1 and P-Smad3 protein expression and increased Smad3 protein expression levels. The present study demonstrated that C/EBPβ has a crucial role in regulating breast cancer cell growth through activating TGF-β-Smad3 signaling. These findings suggest that C/EBPβ may be a potential therapeutic target for breast cancer; however,
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