ArticleMolecular cancer2008
Tuberin haploinsufficiency is associated with the loss of OGG1 in rat kidney tumors.
Article in Molecular cancer, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 23 citations in OpenAlex.
- A novel role of snail in regulating tuberin/AMPK pathways to promote renal fibrosis in the new mouse model of type II diabetes.FASEB bioAdvances · 2021Article
- TP63 Is Significantly Upregulated in Diabetic Kidney.International journal of molecular sciences · 2021Article
- Preclinical evidence of the enhanced effectiveness of combined rapamycin and AICAR in reducing kidney cancer.Molecular oncology · 2018Article
- Novel protective mechanism of reducing renal cell damage in diabetes: Activation AMPK by AICAR increased NRF2/OGG1 proteins and reduced oxidative DNA damage.Cell cycle (Georgetown, Tex.) · 2016Article
- Tuberin-deficiency downregulates N-cadherin and upregulates vimentin in kidney tumor of TSC patients.Oncotarget · 2014Article
- Hyperactivation of Akt/mTOR and deficiency in tuberin increased the oxidative DNA damage in kidney cancer patients with diabetes.Oncotarget · 2014Article
- Novel mechanism of regulation of fibrosis in kidney tumor with tuberous sclerosis.Molecular cancer · 2013Article
- Tuberin inhibits production of the matrix protein fibronectin in diabetes.Journal of the American Society of Nephrology : JASN · 2012Article
- Regulation of PI 3-K, PTEN, p53, and mTOR in Malignant and Benign Tumors Deficient in Tuberin.Genes & cancer · 2011Article
- The tuberin/mTOR pathway promotes apoptosis of tubular epithelial cells in diabetes.Journal of the American Society of Nephrology : JASN · 2011Article
- Novel mechanism of regulation of the DNA repair enzyme OGG1 in tuberin-deficient cells.Carcinogenesis · 2010Article
- Molecular mechanism of regulation of OGG1: tuberin deficiency results in cytoplasmic redistribution of transcriptional factor NF-YA.Journal of molecular signaling · 2009Article
- Insight into mechanism of oxidative DNA damage in angiomyolipomas from TSC patients.Molecular cancer · 2009Article
- Genetics and molecular biology of tuberous sclerosis complex.Current genomics · 2008Article
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Authors and funding
4 authors at 3 institutions in 2 countries.
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Abstract
backgroundTuberous sclerosis complex (TSC) is caused by defects in one of two tumor suppressor genes, TSC-1 or TSC-2. TSC-2 gene encodes tuberin, a protein involved in the pathogenesis of kidney tumors. Loss of heterozygosity (LOH) at the TSC2 locus has been detected in TSC-associated renal cell carcinoma (RCC) and in RCC in the Eker rat. Tuberin downregulates the DNA repair enzyme 8-oxoguanine DNA-glycosylase (OGG1) with important functional consequences, compromising the ability of cells to repair damaged DNA resulting in the accumulation of the mutagenic oxidized DNA, 8-oxo-dG. Loss of function mutations of OGG1 also occurs in human kidney clear cell carcinoma and may contribute to tumorgenesis. We investigated the distribution of protein expression and the activity of OGG1 and 8-oxo-dG and correlated it with the expression of tuberin in kidneys of wild type and Eker rats and tumor from Eker rat.
resultsTuberin expression, OGG1 protein expression and activity were higher in kidney cortex than in medulla or papilla in both wild type and Eker rats. On the other hand, 8-oxo-dG levels were highest in the medulla, which expressed the lowest levels of OGG1. The basal levels of 8-oxo-dG were also higher in both cortex and medulla of Eker rats compared to wild type rats. In kidney tumors from Eker rats, the loss of the second TSC2 allele is associated with loss of OGG1 expression. Immunostaining of kidney tissue shows localization of tuberin and OGG1 mainly in the cortex.
conclusionThese results demonstrate that OGG1 localizes with tuberin preferentially in kidney cortex. Loss of tuberin is accompanied by the loss of OGG1 contributing to tumorgenesis. In addition, the predominant expression of OGG1 in the cortex and its decreased expression and activity in the Eker rat may account for the predominant cortical localization of renal cell carcinoma.
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