{"title":"Progress of Pyruvate Kinase M2 in Hepatocellular Carcinoma-Associated Signaling Pathway.","authors":"Qi Wan, Chunlian Zhao, Rui Zhao","doi":"10.1089/ten.tec.2024.0368","DOIUrl":null,"url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is an aggressive liver tumor with a unique metabolic profile and a shift to glycolytic metabolism. This review discusses the contribution of pyruvate kinase M2 (PKM2) to HCC development and its potential as a target for therapy. We carried out a broad literature review on PKM2, focusing on its role in the glycolytic pathway and special interactions with key signaling pathways like Phosphoinositide 3-kinase/Protein kinase B/Mammalian target of rapamycin (PI3K/AKT/mTOR) and Mitogen-activated protein kinase (MAPK). PKM2 also performs a dual role in energy metabolism and signal transduction in HCC. PKM2 is paramount in the induction of HCC by regulating cellular metabolism and oncogenic signaling pathways. It promotes tumor growth, survival, and metastasis through interaction with the PI3K/AKT/mTOR and MAPK pathways. PKM2 is a key factor in HCC pathogenesis, with a dual impact on metabolism and signaling. Its properties may open the way for developing novel therapeutic interventions against HCC. Thus, PKM2 inhibition may offer further opportunities for tumor growth blockade, which could meaningfully improve patients' clinical outcomes.</p>","PeriodicalId":23154,"journal":{"name":"Tissue engineering. Part C, Methods","volume":"31 3","pages":"101-107"},"PeriodicalIF":2.7000,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Tissue engineering. Part C, Methods","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1089/ten.tec.2024.0368","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"CELL & TISSUE ENGINEERING","Score":null,"Total":0}
引用次数: 0
Abstract
Hepatocellular carcinoma (HCC) is an aggressive liver tumor with a unique metabolic profile and a shift to glycolytic metabolism. This review discusses the contribution of pyruvate kinase M2 (PKM2) to HCC development and its potential as a target for therapy. We carried out a broad literature review on PKM2, focusing on its role in the glycolytic pathway and special interactions with key signaling pathways like Phosphoinositide 3-kinase/Protein kinase B/Mammalian target of rapamycin (PI3K/AKT/mTOR) and Mitogen-activated protein kinase (MAPK). PKM2 also performs a dual role in energy metabolism and signal transduction in HCC. PKM2 is paramount in the induction of HCC by regulating cellular metabolism and oncogenic signaling pathways. It promotes tumor growth, survival, and metastasis through interaction with the PI3K/AKT/mTOR and MAPK pathways. PKM2 is a key factor in HCC pathogenesis, with a dual impact on metabolism and signaling. Its properties may open the way for developing novel therapeutic interventions against HCC. Thus, PKM2 inhibition may offer further opportunities for tumor growth blockade, which could meaningfully improve patients' clinical outcomes.
期刊介绍:
Tissue Engineering is the preeminent, biomedical journal advancing the field with cutting-edge research and applications that repair or regenerate portions or whole tissues. This multidisciplinary journal brings together the principles of engineering and life sciences in the creation of artificial tissues and regenerative medicine. Tissue Engineering is divided into three parts, providing a central forum for groundbreaking scientific research and developments of clinical applications from leading experts in the field that will enable the functional replacement of tissues.
Tissue Engineering Methods (Part C) presents innovative tools and assays in scaffold development, stem cells and biologically active molecules to advance the field and to support clinical translation. Part C publishes monthly.