ArticleThe Journal of biological chemistry2014
Missense mutations in pyruvate kinase M2 promote cancer metabolism, oxidative endurance, anchorage independence, and tumor growth in a dominant negative manner.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Nuclear PKM2: a signal receiver, a gene programmer, and a metabolic modulator.Journal of biomedical science · 2025Review
- HPV18 oncoproteins driven expression of PKM2 reprograms HeLa cell metabolism to maintain aerobic glycolysis and viability.Virusdisease · 2022Article
- TSP50 promotes the Warburg effect and hepatocyte proliferation via regulating PKM2 acetylation.Cell death & disease · 2021Article
- The Role of PKM2 in Metabolic Reprogramming: Insights into the Regulatory Roles of Non-Coding RNAs.International journal of molecular sciences · 2021Review
- Phenotypic selection with an intrabody library reveals an anti-apoptotic function of PKM2 requiring Mitofusin-1.PLoS biology · 2019Article
- Mutations in the PKM2 exon-10 region are associated with reduced allostery and increased nuclear translocation.Communications biology · 2019Article
- Curcumin decreases Warburg effect in cancer cells by down-regulating pyruvate kinase M2 via mTOR-HIF1α inhibition.Scientific reports · 2018Article
- Pkm2 can enhance pluripotency in ESCs and promote somatic cell reprogramming to iPSCs.Oncotarget · 2017Article
- PKM2 and cancer: The function of PKM2 beyond glycolysis.Oncology letters · 2016Article
- Pyruvate kinase M2 at a glance.Journal of cell science · 2015Review
- Structural basis of PKM2 regulation.Protein & cell · 2015Article
- Structural insight into mechanisms for dynamic regulation of PKM2.Protein & cell · 2015Article
- mtDNA germ line variation mediated ROS generates retrograde signaling and induces pro-cancerous metabolic features.Scientific reports · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study was designed to examine the functional relevance of two heterozygous mutations (H391Y and K422R), observed earlier by us in the Bloom syndrome condition. Cells stably expressing exogenous wild-type or mutant PKM2 (K422R or H391Y) or co-expressing both wild type and mutant (PKM2-K422R or PKM2-H391Y) were assessed for cancer metabolism and tumorigenic potential. Interestingly, cells co-expressing PKM2 and mutant (K422R or H391Y) showed significantly aggressive cancer metabolism as compared with cells expressing either wild-type or mutant PKM2 independently. A similar trend was observed for oxidative endurance, tumorigenic potential, cellular proliferation, and tumor growth. These observations signify the dominant negative nature of mutations. Remarkably, PKM2-H391Y co-expressed cells showed a maximal effect on all the studied parameters. Such a dominant negative impaired function of PKM2 in tumor development is not known; this study demonstrates for the first time the possible predisposition of Bloom syndrome patients with impaired PKM2 activity to cancer and the importance of studying genetic variations in PKM2 in the future to understand their relevance in cancer in general.
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