ArticleCancer & metabolism2023
Restoring gluconeogenesis by TEF inhibited proliferation and promoted apoptosis and immune surveillance in kidney renal clear cell carcinoma.
Article in Cancer & metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 3 citations in OpenAlex.
- Comprehensive pan-cancer analysis of AARS1, a newly identified lactyltransferase in human cancers.Cancer cell international · 2026Article
- Combining single-cell and bulk RNA sequencing data to create a reliable prognostic model for predicting clear-cell renal cell carcinoma progression.Translational andrology and urology · 2025Article
- Single-cell sequencing technology in renal cancer: insights into tumor biology and clinical application.Biomarker research · 2025Review
- Tanshinone I improves renal fibrosis by promoting gluconeogenesis through upregulation of peroxisome proliferator-activated receptor-γ coactivator 1α.Renal failure · 2024Article
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Authors and funding
4 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundKidney renal clear cell carcinoma (KIRC) is the major histological subtype of kidney tumor which covers approximately 80% of the cases. Although various therapies have been developed, the clinical outcome remains unsatisfactory. Metabolic dysregulation is a key feature of KIRC, which impacts progression and prognosis of the disease. Therefore, understanding of the metabolic changes in KIRC is of great significance in improving the treatment outcomes.
methodsThe glycolysis/gluconeogenesis genes were analyzed in the KIRC transcriptome from the Cancer Genome Atlas (TCGA) by the different expression genes (DEGs) test and survival analysis. The gluconeogenesis-related miRNAs were identified by ImmuLncRNA. The expression levels of indicated genes and miRNAs were validated in KIRC tumor and adjunct tissues by QPCR. The effects of miR-4477b and PCK1 on cell proliferation and apoptosis were examined using the cell viability assay, cell apoptosis assay, and clone information. The interaction of miR-4477b with TEF was tested by the luciferase report gene assay. The different gluconeogenesis statuses of tumor cells and related signatures were investigated by single-cell RNA sequencing (scRNA-seq) analysis.
resultsThe 11 gluconeogenesis genes were found to be suppressed in KIRC (referring as PGNGs), and the less suppression of PGNGs indicated better survival outcomes. Among the 11 PGNGs, we validated four rate-limiting enzyme genes in clinical tumor patients. Moreover, restoring gluconeogenesis by overexpressing PCK1 or TEF through miR-4477b inhibition significantly inhibited tumor cell proliferation, colony formation, and induced cell apoptosis in vitro. Independent single-cell RNA sequencing (scRNA-seq) data analysis revealed that the tumor cells had high levels of PGNG expression (PGNG + tumor cells) represented a phenotype of early stage of neoplasia and prompted immune surveillance.
conclusionsOur study suggests that the deficiency of gluconeogenesis is a key metabolic feature of KIRC, and restoring gluconeogenesis could effectively inhibit the proliferation and progression of KIRC cells.
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