ArticleAmerican journal of cancer research2023
Mitochondrial phosphoenolpyruvate carboxykinase inhibits kidney renal clear cell carcinoma malignant progression, leading to cell energy metabolism imbalance.
Article in American journal of cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 5 citations in OpenAlex.
- PCK2 Promotes Ribosome Biogenesis in Cervical Cancer Cells via Interaction with hnRNPK.Reproductive sciences (Thousand Oaks, Calif.) · 2026Article
- Phosphoenolpyruvate carboxykinase 2 as a prognostic biomarker: expression and clinical significance in Group 3 and Group 4 medulloblastoma.Journal of neuro-oncology · 2026Article
- Unveiling diagnostic biomarkers and therapeutic targets in lung adenocarcinoma using bioinformatics and experimental validation.Scientific reports · 2025Article
- Lactylation-Driven IGF2BP3-Mediated Serine Metabolism Reprogramming and RNA m6A-Modification Promotes Lenvatinib Resistance in HCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The gluconeogenesis enzyme PCK2 has a non-enzymatic role in proteostasis in endothelial cells.Communications biology · 2024Article
- Phosphoenolpyruvate carboxykinase 2-mediated metabolism promotes lung tumorigenesis by inhibiting mitochondrial-associated apoptotic cell death.Frontiers in pharmacology · 2024Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial phosphoenolpyruvate carboxykinase (PCK2) is a key gluconeogenesis enzyme. Its differential expression is related to kidney renal clear cell carcinoma (KIRC) malignancy, possibly by influencing energy metabolism. Therefore, it is possible that PKC2 plays a significant part in the emergence and progression of KIRC. To systematically and comprehensively identify the significance of PCK2 in KIRC, we further studied PCK2 in terms of its relationship to clinical features and various clinical subgroups' prognoses. Moreover, we verified the effect of PCK2 and KIRC cells using experimental methods. PCR and western blotting analyses confirmed PCK2 expression in KIRC cell lines and tissues. As a cell model, we constructed cells that overexpress PCK2. Proliferation was detected by EdU experiments. Scratch tests and transwell assays were used, respectively, to analyze cell migration and invasion. Mass spectrometry detected energy metabolite expression in KIRC cells. The findings revealed that KIRC patients with lower levels of PCK2 expression exhibited shorter progression-free intervals, shorter disease-specific survival, and shorter overall survival. The experimental results showed that compared with 293t, PCK2 was downregulated in three KIRC lines (OSRC-2, 786-O, and A498). Relative to surrounding tissues, PCK2 was downregulated in KIRC. PCK2 overexpression inhibited KIRC cell proliferation, migration, and invasion and upregulated energy metabolite expression. Mass spectrometry revealed that thiamine pyrophosphate, cyclic AMP, beta-D-fructose 6-phosphate, lactate, flavin mononucleotide, NAD, NADP, and D-glucose 6-phosphate were upregulated. PCK2 has the potential to serve as both a diagnostic and prognostic molecular biomarker for KIRC, as well as an independent prognostic risk factor for KIRC. It is hoped that PCK2 will emerge as a therapeutic target for KIRC.
Indexed as
Identifiers
37034209PMC10077028W4363646248What OpenQuestion holds
Registered trials
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