ArticleOncotarget2017
Overexpression of HSD17B4 exerts tumor suppressive function in adrenocortical carcinoma and is not associated with hormone excess.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Deciphering 17-β-hydroxysteroid dehydrogenase 4: from molecular insights to cancer therapeutics.Cancer cell international · 2025Review
- Gamma-tocotrienol Inhibits Proliferation and Growth of HSD17B4 Overexpressing HepG2 Liver Cancer Cells.Current cancer drug targets · 2025Article
- Estradiol and Estrone Have Different Biological Functions to Induce NF-κB-Driven Inflammation, EMT and Stemness in ER+ Cancer Cells.International journal of molecular sciences · 2023Article
- High expression of peroxisomal D-bifunctional protein in cytosol regulates apoptosis and energy metabolism of hepatocellular carcinoma cells via PI3K/AKT pathway.American journal of cancer research · 2023Article
- Salivary Exosome Proteomics and Bioinformatics Analysis in 7,12-Dimethylbenz[a]anthracene-Induced Oral Cancer with Radiation Therapy-A Syrian Golden Hamster Model.Diagnostics (Basel, Switzerland) · 2021Article
- HSD17B4, ACAA1, and PXMP4 in Peroxisome Pathway Are Down-Regulated and Have Clinical Significance in Non-small Cell Lung Cancer.Frontiers in genetics · 2020Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimAdrenocortical carcinoma (ACC) is characterized with excessive hormone production. We therefore investigated expression of hormone-related genes in ACC.
resultsWe queried status of 14 key genes directly involved in adrenal hormone production and found HSD17B4 expression was upregulated in 39% of ACC cases on top of all queried genes. Overexpression of HSD17B4 was significantly associate with a normo-hormonal phenotype. Constitutive HSD17B4 expression was higher in ACC cell line NCI-H295R than in adrenocortical small cell carcinoma cell line SW13. NCI-H295R cells with HSD17B4-knockdown (KD) demonstrated significantly inhibited proliferation, increased apoptosis, and increased cell cycle arrest. Enrichment analysis for mRNA expression in ACC samples with or without HSD17B4 overexpression showed significant change in p53 pathway. Replenish of HSD17B4 in SW13 cells and knockdown of HSD17B4 in H295R cells confirmed alterations in MDM4, ATR, and IE24 with alterations more contrasting in H295R cells. HSD17B4-KD inhibited cell invasion, migration and anchorage independent growth of NCI-H295R cells, but not of SW13 cells. MATERIALS AND
methodsClinical and genetic data of ACC samples were reproduced from the ACC dataset of The Cancer Genome Atlas (TCGA) database using cBioPortal. Genes participating in adrenal hormone production were queried. Association between gene status and hormone release were studied and
conclusionsOverexpression of HSD17B4 exerted tumor suppressive function in adrenocortical carcinoma and was not related to hormone excess. Crosstalk between HSD17B4 and p53 warrants further investigation.
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