ArticleCell death & disease2022
AK2 is an AMP-sensing negative regulator of BRAF in tumorigenesis.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Whole exome sequencing identifies somatically mutated genes in bladder cancer: A pilot study from Bangladesh.Biochemistry and biophysics reports · 2026Article
- Machine learning-based prognostic signature integrating mitochondrial function and programmed cell death patterns in pancreatic adenocarcinoma.Scientific reports · 2026Article
- Mitochondrial AK3 inhibits nuclear β-catenin localization and its activation through enhancing mitochondrial activity.Cell death & disease · 2026Article
- Resistance Training and Resveratrol Supplementation Improve Cancer Cachexia and Tumor Volume in Muscle Tissue of Male Mice Bearing Colon Cancer CT26 Cell Tumors.Cell biochemistry and biophysics · 2025Article
- Adenylate kinase 2 is a biomarker related to the prognosis of glioma and the immune microenvironment.Journal of clinical laboratory analysis · 2023Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RAS-BRAF signaling is a major pathway of cell proliferation and their mutations are frequently found in human cancers. Adenylate kinase 2 (AK2), which modulates balance of adenine nucleotide pool, has been implicated in cell death and cell proliferation independently of its enzyme activity. Recently, the role of AK2 in tumorigenesis was in part elucidated in some cancer types including lung adenocarcinoma and breast cancer, but the underlying mechanism is not clear. Here, we show that AK2 is a BRAF-suppressor. In in vitro assays and cell model, AK2 interacted with BRAF and inhibited BRAF activity and downstream ERK phosphorylation. Energy-deprived conditions in cell model and the addition of AMP to cell lysates strengthened the AK2-BRAF interaction, suggesting that AK2 is involved in the regulation of BRAF activity in response to cell metabolic state. AMP facilitated the AK2-BRAF complex formation through binding to AK2. In a panel of HCC cell lines, AK2 expression was inversely correlated with ERK/MAPK activation, and AK2-knockdown or -knockout increased BRAF activity and promoted cell proliferation. Tumors from HCC patients showed low-AK2 protein expression and increased ERK activation compared to non-tumor tissues and the downregulation of AK2 was also verified by two microarray datasets (TCGA-LIHC and GSE14520). Moreover, AK2/BRAF interaction was abrogated by RAS activation in in vitro assay and cell model and in a mouse model of HRAS
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