ArticleJournal of translational medicine2022
SPTBN1 abrogates renal clear cell carcinoma progression via glycolysis reprogramming in a GPT2-dependent manner.
Article in Journal of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Neurexophilin 4 facilitates the malignant progression of kidney renal clear cell carcinoma by regulating PI3K/AKT-mediated glycolysis.Molecular genetics and genomics : MGG · 2026Article
- HBx-mediated GPT2 suppression promotes liver cancer development by downregulating ADH1A.Cancer biology & medicine · 2026Article
- Exploring the Effects of Teas with Different Fermentation Levels and Black Coffee on the Body via the Urine Proteome.Nutrients · 2026Article
- CLCluster: A redundancy-reduction contrastive learning-based clustering method of cancer subtype based on multi-omics data.Molecular therapy. Nucleic acids · 2025Article
- Targeting HVEM-GPT2 axis: a novel approach to T cell activation and metabolic reprogramming in non-small cell lung cancer therapy.Cancer immunology, immunotherapy : CII · 2025Article
- Article
- Solute carrier family 6 member 3 promotes the development of clear cell renal cell carcinoma by enhancing glycolysis and inhibiting ferroptosis.CytoJournal · 2025Article
- The role of BUD31 in clear cell renal cell carcinoma: prognostic significance, alternative splicing, and tumor immune environment.Clinical and experimental medicine · 2024Article
- Metabolism-regulated ferroptosis in cancer progression and therapy.Cell death & disease · 2024Review
- Article
- Analysis and Verification of Glycosylation Characteristics of Septic Acute Kidney Injury.Journal of inflammation research · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRenal clear cell carcinoma (ccRCC) is the most prevalent tumors worldwide. Discovering effective biomarkers is essential to monitor the prognosis and provide alternative clinical options. SPTBN1 is implicated in various cancerous processes. However, its role in ccRCC remains unelucidated. This study intends to explore the biological function and mechanism of SPTBN1 in ccRCC.
methodsSingle-cell and bulk RNA-seq, tissue microarray, real-time quantitative PCR, and western blotting were applied to verify the expression and predictive value of SPTBN1 in ccRCC. Gain or loss of functional ccRCC cell line models were constructed, and in vitro and in vivo assays were performed to elucidate its tumorigenic phenotypes. Actinomycin D experiment, RNA immunoprecipitation (RIP), specific inhibitors, and rescue experiments were carried out to define the molecular mechanisms.
resultsSPTBN1 was down-regulated in ccRCC and knockdown of SPTBN1 displayed a remarkably oncogenic role both in vitro and in vivo; while overexpressing SPTBN1 reversed this effect. SPTBN1 mediated ccRCC progression via the pathway of glutamate pyruvate transaminase 2 (GPT2)-dependent glycolysis. The expression of GPT2 was significantly negatively correlated with that of SPTBN1. As an RNA binding protein SPTBN1, regulated the mRNA stability of GPT2.
conclusionOur research demonstrated that SPTBN1 is significantly down-regulated in ccRCC. SPTBN1 knockdown promotes ccRCC progression via activating GPT2-dependent glycolysis. SPTBN1 may serve as a therapeutic target for the treatment of ccRCC.
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