ArticleJournal of translational medicine2020
ABAT and ALDH6A1, regulated by transcription factor HNF4A, suppress tumorigenic capability in clear cell renal cell carcinoma.
Article in Journal of translational medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
- Renal proteomics of male offspring exposed to maternal protein restriction: molecular, epigenetic, and nephron-specific signatures of metabolic programming.Journal of physiology and biochemistry · 2026Article
- Gamma-aminobutyric acid transaminase mediates tumor suppression in renal cell carcinoma through the cGAS-STING-interferon-β axis.Scientific reports · 2026Article
- ALDH2 in autophagy and cell death: molecular mechanisms and implications for diseases.Military Medical Research · 2025Review
- Propionate metabolism-related genes demonstrate the potential to serve as prognostic and immunotherapeutic markers in osteosarcoma.Oncology letters · 2025Article
- GABA regulates metabolic reprogramming to mediate the development of brain metastasis in non-small cell lung cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Identifying ADME-related gene signature for immune landscape and prognosis in KIRC by single-cell and spatial transcriptome analysis.Scientific reports · 2025Article
- The double role of GABAergic system in systemic tumors: an updated review.Frontiers in oncology · 2025Review
- Modeling metabolic-associated steatohepatitis with human pluripotent stem cell-derived liver organoids.Hepatology communications · 2024Article
- Modal-nexus auto-encoder for multi-modality cellular data integration and imputation.Nature communications · 2024Article
- Targeting the peripheral neural-tumour microenvironment for cancer therapy.Nature reviews. Drug discovery · 2024Review
- Article
- Research on molecular characteristics of ADME-related genes in kidney renal clear cell carcinoma.Scientific reports · 2024Article
- Decoding sunitinib resistance in ccRCC: Metabolic-reprogramming-induced ABAT and GABAergic system shifts.iScience · 2024Article
- Chromosome-level Asian elephant genome assembly and comparative genomics of long-lived mammals reveal the common substitutions for cancer resistance.Aging cell · 2023Article
- Insights into the leveraging of GABAergic signaling in cancer therapy.Cancer medicine · 2023Review
- Identification and validation of NFIA as a novel prognostic marker in renal cell carcinoma.The journal of pathology. Clinical research · 2023Article
- An in vitro approach to understand contribution of kidney cells to human urinary extracellular vesicles.Journal of extracellular vesicles · 2023Article
- Aldehyde dehydrogenase in solid tumors and other diseases: Potential biomarkers and therapeutic targets.MedComm · 2023Review
- An immune infiltration-related prognostic model of kidney renal clear cell carcinoma with two valuable markers: CAPN12 and MSC.Frontiers in oncology · 2023Article
- Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundClear cell renal cell carcinoma (ccRCC) is a malignancy characterized by metabolic reprogramming. ABAT and ALDH6A1 are metabolic enzymes. In this study, we aim to investigate the associations of ABAT and ALDH6A1 with the malignancy of ccRCC cells.
methodsThe gene expression levels of ABAT and ALDH6A1 in ccRCC were analyzed from gene expression microarray datasets and RNA sequencing data. Clinical information was analyzed from The Cancer Genome Atlas (TCGA) data. The distributions of ABAT and ALDH6A1 in ccRCC clinical tissues were screened by reverse transcription-quantitative polymerase chain reaction (RT-QPCR) and immunohistochemical assays. The effect of overexpression of ABAT or ALDH6A1 was measured by detecting the cell viability, migration ability, and the ratio of lactate and nicotinamide adenine dinucleotide phosphate (NADPH). Chromatin immunoprecipitation (ChIP) and luciferase reporter assays were carried out to investigate the transcript regulation of HNF4A in ABAT and ALDH6A1.
resultsRemarkable downregulated ABAT and ALDH6A1 expression levels were observed in ccRCC patients and low expression of ABAT and ALDH6A1 was correlated with poor survival. Overexpression of ABAT or ALDH6A1 significantly attenuated cell proliferation and migration, and impaired lactate production. In ABAT increased ccRCC cells, the ratio of NADPH/NADP+ was reduced. Finally, we demonstrated that ABAT and ALDH6A1 were directly regulated by a tumor suppressor, HNF4A.
conclusionsThese observations identified HNF4A-regulated low-expressed ABAT and ALDH6A1 as promising diagnostic and prognostic biomarkers for ccRCC.
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