ArticleCancer biology & therapy2008
Inhibition of Mxi1 suppresses HIF-2alpha-dependent renal cancer tumorigenesis.
Article in Cancer biology & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Epigenetic and transcriptomic characterization reveals progression markers and essential pathways in clear cell renal cell carcinoma.Nature communications · 2023Article
- ADD3 Deletion in Glioblastoma Predicts Disease Status and Survival.Frontiers in oncology · 2021Article
- Integrating transcriptional and protein interaction networks to prioritize condition-specific master regulators.BMC systems biology · 2015Article
- Functional interactions among members of the MAX and MLX transcriptional network during oncogenesis.Biochimica et biophysica acta · 2015Review
- MYC degradation under low O2 tension promotes survival by evading hypoxia-induced cell death.Molecular and cellular biology · 2013Article
- Article
- Statistical methods for gene set co-expression analysis.Bioinformatics (Oxford, England) · 2009Article
- The role of MXI1 in VHL deficient tumorigenesis.Cancer biology & therapy · 2008Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In clear cell renal cancers, the primary molecular defect is inactivation of the von Hippel-Lindau (VHL) gene. Loss of pVHL, the VHL gene product, leads to constitutive activation of hypoxia-inducible factor (HIF) signaling. While downregulation of HIF suppresses tumor formation by pVHL-defective renal carcinoma cells, the relative contribution of individual HIF regulated genes to HIF-dependent tumorigenesis remains under investigation. Mxi1, a c-Myc antagonist, is a HIF target gene that inhibits mitochondrial biogenesis, reprograms cellular energy metabolism, and protects cells from c-Myc-dependent apoptosis in vitro. In the present study we show that Mxi1 is overexpressed in primary human clear cell kidney cancers. Inhibition of Mxi1 in pVHL-defective kidney cancer cells using shRNA alters their cell cycle parameters, inhibits their ability to invade matrigel, and suppresses their ability to form tumors in vivo. Compared to Mxi1-proficient tumors, Mxi1-deficient tumors display reduced cellular proliferation. These results establish Mxi1 as an important downstream target of HIF that contributes to pVHL-deficient renal cancer tumorigenesis.
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