ArticleCancer medicine2023
Tumor protein D52 (TPD52) affects cancer cell metabolism by negatively regulating AMPK.
Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Integrative phosphoproteomic network analysis identifies CAMK2D as a shared regulator of TPD52 family proteins in cancer.Protoplasma · 2026Article
- Unpacking the Tumor Protein D52-like Family: Roles in Intracellular Trafficking and Cancer Progression.Cells · 2026Review
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- TPD52 is a Potential Prognostic Biomarker and Correlated with Immune Infiltration: A Pan-cancer Analysis.Current molecular medicine · 2024Article
- Circular RNA circEZH2 Promotes Lung Adenocarcinoma Progression by Regulating microRNA-495-3p/Tumor Protein D52 Axis and Activating Nuclear Factor-Kappa B Pathway.International journal of general medicine · 2024Article
- Investigation of risk signatures associated with anoikis in thyroid cancer through integrated transcriptome and Mendelian randomization analysis.Frontiers in endocrinology · 2024Article
- Cross talk of tumor protein D52 (TPD52) with KLF9, PKCε, and MicroRNA 223 in ovarian cancer.Journal of ovarian research · 2023Article
- AMPK targets a proto-oncogene TPD52 (isoform 3) expression and its interaction with LKB1 suppress AMPK-GSK3β signaling axis in prostate cancer.Journal of cell communication and signaling · 2023Article
- Tumor protein D52 (TPD52) affects cancer cell metabolism by negatively regulating AMPK.Cancer medicine · 2023Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundThe AMP-activated protein kinase (AMPK) is a central regulator of energy homeostasis, with deregulation leading to cancer and other diseases. However, how this pathway is dysregulated in cancer has not been well clarified.
methodsUsing a tandem affinity purification/mass-spec technique and biochemical analyses, we identified tumor protein D52 (TPD52) as an AMPKα-interacting molecule. To explore the biological effects of TPD52 in cancers, we conducted biochemical and metabolic assays in vitro and in vivo with cancer cells and TPD52 transgenic mice. Finally, we assessed the clinical significance of TPD52 expression in breast cancer patients using bioinformatics techniques.
resultsTPD52, initially identified to be overexpressed in many human cancers, was found to form a stable complex with AMPK in cancer cells. TPD52 directly interacts with AMPKα and inhibits AMPKα kinase activity in vitro and in vivo. In TPD52 transgenic mice, overexpression of TPD52 leads to AMPK inhibition and multiple metabolic defects. Clinically, high TPD52 expression predicts poor survival of breast cancer patients.
conclusionThe findings revealed that TPD52 is a novel regulator of energy stress-induced AMPK activation and cell metabolism. These results shed new light on AMPK regulation and understanding of the etiology of cancers with TPD52 overexpression.
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