ArticleMolecular biology of the cell2008
Transcriptional regulation of serine/threonine kinase-15 (STK15) expression by hypoxia and HIF-1.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Aurora-A activation, correlated with hypoxia-inducible factor-1α, promotes radiochemoresistance and predicts poor outcome for nasopharyngeal carcinoma.Cancer science · 2012Trial
- Anoxia tolerant DNA replication is supported by ATR kinase in the annual killifish Austrofundulus limnaeus.Journal of cell science · 2026Article
- Tumour hypoxia in driving genomic instability and tumour evolution.Nature reviews. Cancer · 2025Review
- Functional Repercussions of Hypoxia-Inducible Factor-2α in Idiopathic Pulmonary Fibrosis.Cells · 2022Review
- Regulating the regulator: a survey of mechanisms from transcription to translation controlling expression of mammalian cell cycle kinase Aurora A.Open biology · 2022Review
- Adaptation to Hypoxia May Promote Therapeutic Resistance to Androgen Receptor Inhibition in Triple-Negative Breast Cancer.International journal of molecular sciences · 2022Review
- Hypoxia Drives Centrosome Amplification in Cancer Cells via HIF1α-dependent Induction of Polo-Like Kinase 4.Molecular cancer research : MCR · 2022Article
- Role of Hypoxia in the Control of the Cell Cycle.International journal of molecular sciences · 2021Review
- Article
- Identification of molecular target genes and key pathways in hepatocellular carcinoma by bioinformatics analysis.OncoTargets and therapy · 2018Article
- Hypoxia inducible factors in hepatocellular carcinoma.Oncotarget · 2017Review
- Hypoxia-inducible factor prolyl hydroxylase 2 (PHD2) is a direct regulator of epidermal growth factor receptor (EGFR) signaling in breast cancer.Oncotarget · 2017Article
- Transcription factor HIF1A: downstream targets, associated pathways, polymorphic hypoxia response element (HRE) sites, and initiative for standardization of reporting in scientific literature.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- A MYC-aurora kinase A protein complex represents an actionable drug target in p53-altered liver cancer.Nature medicine · 2016Article
- Aurora kinase A in gastrointestinal cancers: time to target.Molecular cancer · 2015Review
- β-catenin links von Hippel-Lindau to aurora kinase A and loss of primary cilia in renal cell carcinoma.Journal of the American Society of Nephrology : JASN · 2015Article
- RNA-seq reveals aurora kinase-driven mTOR pathway activation in patients with sarcomatoid metastatic renal cell carcinoma.Molecular cancer research : MCR · 2015Article
- Prognosis value of mitotic kinase Aurora-A for primary duodenal adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Targeting aurora kinase A inhibits hypoxia-mediated neuroblastoma cell tumorigenesis.Anticancer research · 2014Article
- The role of Aurora A in hypoxia-inducible factor 1α-promoting malignant phenotypes of hepatocelluar carcinoma.Cell cycle (Georgetown, Tex.) · 2013Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The serine/threonine kinase-15 (STK15) acts as a cell cycle regulator being overexpressed in various tumors. One mechanism that could contribute to overexpression of STK15 is tumor hypoxia where hypoxia-inducible factor-1 (HIF-1) is a major regulator of transcription. Therefore, we analyzed whether hypoxia and HIF-1 could contribute to overexpression of STK15. We found that hypoxia increased STK15 expression and STK15 promoter activity in HepG2 tumor cells. Overexpression of HIF-1 alpha induced STK15 gene transcription, whereas HIF-1 alpha siRNA and overexpression of prolyl hydroxylase 2 (PHD-2), a negative regulator of HIF-1 alpha, reversed this effect. In addition, site-directed mutagenesis experiments and chromatin immunoprecipitation revealed that from the three putative hypoxia responsive elements (HRE) within the STK15 promoter only HRE-2 was functional and bound HIF-1. Further, siRNA against STK15 inhibited proliferation of HepG2 cells induced by hypoxia. These results show that STK15 gene transcription can be regulated by hypoxia and HIF-1 via HRE-2 of the STK15 promoter. Thus, tumor hypoxia may trigger overexpression of STK15 observed in various tumors.
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