ArticleMedical oncology (Northwood, London, England)2011
CIDE-3 interacts with lipopolysaccharide-induced tumor necrosis factor, and overexpression increases apoptosis in hepatocellular carcinoma.
Article in Medical oncology (Northwood, London, England), 2011. 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, 15 citations in OpenAlex.
- Lipid droplet-associated proteins: Roles in cardiovascular diseases.Journal of lipid research · 2026Review
- CIDEB promotes lipid deposition in goat intramuscular adipocytes.Animal bioscience · 2025Article
- Decoding 17-Beta-hydroxysteroid Dehydrogenase 13: A Multifaceted Perspective on Its Role in Hepatic Steatosis and Associated Disorders.Journal of clinical and translational hepatology · 2024Review
- Exploring the impact of lipid droplets on the evolution and progress of hepatocarcinoma.Frontiers in cell and developmental biology · 2024Review
- Adding fuel to the fire: The lipid droplet and its associated proteins in cancer progression.International journal of biological sciences · 2022Review
- Epigenome-wide association study of asthma and wheeze characterizes loci withinAllergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2019Article
- Silencing ofFrontiers in cell and developmental biology · 2019Article
- Role of glycoprotein 78 and cidec in hepatic steatosis.Molecular medicine reports · 2017Article
- Gene expression changes in tumor free tongue tissue adjacent to tongue squamous cell carcinoma.Oncotarget · 2017Article
- The feedback loop of LITAF and BCL6 is involved in regulating apoptosis in B cell non-Hodgkin's-lymphoma.Oncotarget · 2016Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell death-inducing DFF45-like effector-3 (CIDE-3) is a novel member of an apoptosis-inducing protein family, but its function is unknown. CIDE-3 shows a different distribution pattern in hepatocellular carcinoma (HCC) tissues and normal adjacent tissues. Therefore, this work tested the hypothesis that CIDE-3 induces apoptosis in HCC cells, inhibiting oncogenesis and tumor development. We used immunohistochemistry to evaluate the expression of CIDE-3 in 82 HCC samples and 51 adjacent liver tissues. Overexpression of CIDE-3 induced apoptosis, as detected by flow cytometry, in the HCC cell line SMMC-7721, which had undetectable levels of CIDE-3 in the absence of CIDE-3 overexpression. A yeast two-hybrid system was employed to screen for proteins that interact with CIDE-3. The expression of CIDE-3 was decreased in HCC tissue, compared to adjacent normal tissues, and CIDE-3 expression and HCC differentiation were positively correlated. CIDE-3 expression levels were lower in poorly differentiated HCC tissue than in well-differentiated HCC tissue. Overexpressed CIDE-3 inhibited proliferation and induced apoptosis in HCC cells. We found that lipopolysaccharide-induced tumor necrosis factor (LITAF) interacted with CIDE-3 in hepatic cells. This is the first demonstrated interaction between CIDE-3 and LITAF, and the first report that CIDE-3 induces apoptosis in hepatocellular carcinoma.
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