ArticleCancer science2017
Enhanced expression of the M2 isoform of pyruvate kinase is involved in gastric cancer development by regulating cancer-specific metabolism.
Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- Glycolysis‑driven immunosuppression in gastric cancer: Metabolic crosstalk between tumor cells and the immune microenvironment (Review).International journal of oncology · 2026Review
- Review
- Mechanisms of Metabolic Reprogramming Regulating Immunosuppression in the Gastric Cancer Tumor Microenvironment.Biomolecules · 2026Review
- Metabolic reprogramming as a key regulator in Helicobacter pylori-infected gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Review
- Unveiling Metabolic Signatures as Potential Biomarkers in Common Cancers: Insights from Lung, Breast, Colorectal, Liver, and Gastric Tumours.Biomolecules · 2025Review
- All-trans-retinoic acid modulates glycolysis via H19 and telomerase: the role of mir-let-7a in estrogen receptor-positive breast cancer cells.BMC cancer · 2024Article
- Targeting the Metabolic Paradigms in Cancer and Diabetes.Biomedicines · 2024Review
- USP4 promotes the proliferation and glucose metabolism of gastric cancer cells by upregulating PKM2.PloS one · 2023Article
- CagA and VacA inhibit gastric mucosal epithelial cell autophagy and promote the progression of gastric precancerous lesions.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Candidate therapeutic agents in a newly established triple wild-type mucosal melanoma cell line.Cancer communications (London, England) · 2022Article
- Glycolysis in the progression of pancreatic cancer.American journal of cancer research · 2022Review
- Down-regulation of NOTCH1 and PKM2 can inhibit the growth and metastasis of colorectal cancer cells.American journal of translational research · 2022Article
- A Novel Necroptosis-Related Gene Signature in Skin Cutaneous Melanoma Prognosis and Tumor Microenvironment.Frontiers in genetics · 2022Article
- Identification of 14 Differentially-Expressed Metabolism-Related Genes as Potential Targets of Gastric Cancer by Integrated Proteomics and Transcriptomics.Frontiers in cell and developmental biology · 2022Article
- Nanoparticle-Encapsulated Camptothecin: Epigenetic Modulation in DNA Repair Mechanisms in Colon Cancer Cells.Molecules (Basel, Switzerland) · 2021Article
- Tumor pyruvate kinase M2 modulators: a comprehensive account of activators and inhibitors as anticancer agents.RSC medicinal chemistry · 2021Review
- Discovery of Functional Alternatively SplicedCancers · 2021Article
- The Crosstalk Between Signaling Pathways and Cancer Metabolism in Colorectal Cancer.Frontiers in pharmacology · 2021Review
- Gastric Cancer Stem Cells: A Glimpse on Metabolic Reprogramming.Frontiers in oncology · 2021Review
- Alternative Splicing: Expanding the Landscape of Cancer Biomarkers and Therapeutics.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have indicated that increased expression of the M2 isoform of pyruvate kinase (PKM2) is involved in glycolysis and tumor development. However, little is known about the role of PKM2 in gastric cancer (GC). Therefore, we examined the expression and function of PKM2 in human GC. We evaluated PKM1 and PKM2 expression by quantitative RT-PCR in gastric tissues from 10 patients who underwent gastric endoscopic submucosal dissection, 80 patients who underwent gastrectomy, and seven healthy volunteers, and analyzed the correlation with clinicopathological variables. To assess the function of PKM2, we generated PKM2-knockdown GC cells, and investigated the phenotypic changes. Furthermore, we examined the induction of PKM2 expression by cytotoxin-associated gene A (CagA), a pathogenic factor of Helicobacter pylori, using CagA-inducible GC cells. We found that PKM2 was predominantly expressed not only in GC lesions but also in the normal gastric regions of GC patients and in the gastric mucosa of healthy volunteers. The PKM2 expression was significantly higher in carcinoma compared to non-cancerous tissue and was associated with venous invasion. Knockdown of PKM2 in GC cells caused significant decreases in cellular proliferation, migration, anchorage-independent growth, and sphere formation in vitro, and in tumor growth and liver metastasis in vivo. The serine concentration-dependent cell proliferation was also inhibited by PKM2 silencing. Furthermore, we found that PKM2 expression was upregulated by CagA by way of the Erk pathway. These results suggested that enhanced PKM2 expression plays a pivotal role in the carcinogenesis and development of GC in part by regulating cancer-specific metabolism.
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