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      Pyruvate kinase M2 (PKM2) in cancer and cancer therapeutics.

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          Abstract

          Pyruvate kinase M2 (PKM2), a key rate-limiting enzyme of glycolysis, is a critical regulator in tumor metabolism. PKM2 has been demonstrated to overexpressed in various cancers and promoted proliferation and metastasis of tumor cells. The errant expression of PKM2 has inspired people to investigate the function of PKM2 and the therapeutic potential in cancer. In addition, some studies have shown that the upregulation of PKM2 in tumor tissues is associated with the altered expression of lncRNAs and the poor survival. Therefore, researchers have begun to unravel the specific molecular mechanisms of lncRNA-mediated PKM2 expression in cancer metabolism. As the tumor microenvironment (TME) is essential in tumor development, it is necessary to identify the role of PKM2 in TME. In this review, we will introduce the role of PKM2 in different cancers as well as TME, and summarize the molecular mechanism of PKM2-related lncRNAs in cancer metabolism. We expect that this work will lead to a better understanding of the molecular mechanisms of PKM2 that may help in developing therapeutic strategies in clinic for researchers.

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          Author and article information

          Journal
          Cancer Lett
          Cancer letters
          Elsevier BV
          1872-7980
          0304-3835
          Apr 10 2021
          : 503
          Affiliations
          [1 ] Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China; Hunan Key Laboratory of Skin Cancer and Psoriasis, Changsha, Hunan, China; Hunan Engineering Research Center of Skin Health and Disease, Changsha, Hunan, China; Xiangya Clinical Research Center for Cancer Immunotherapy, Central South University, Changsha, Hunan, China; Research Center of Molecular Metabolomics, Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, Hunan, China.
          [2 ] Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China; Hunan Key Laboratory of Skin Cancer and Psoriasis, Changsha, Hunan, China; Hunan Engineering Research Center of Skin Health and Disease, Changsha, Hunan, China; Xiangya Clinical Research Center for Cancer Immunotherapy, Central South University, Changsha, Hunan, China; Research Center of Molecular Metabolomics, Xiangya Hospital, Central South University, Changsha, Hunan, China.
          [3 ] Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China; Hunan Key Laboratory of Skin Cancer and Psoriasis, Changsha, Hunan, China; Hunan Engineering Research Center of Skin Health and Disease, Changsha, Hunan, China; Xiangya Clinical Research Center for Cancer Immunotherapy, Central South University, Changsha, Hunan, China; Research Center of Molecular Metabolomics, Xiangya Hospital, Central South University, Changsha, Hunan, China. Electronic address: chenxiangck@126.com.
          [4 ] Department of Dermatology, Xiangya Hospital, Central South University, Changsha, Hunan, China; Hunan Key Laboratory of Skin Cancer and Psoriasis, Changsha, Hunan, China; Hunan Engineering Research Center of Skin Health and Disease, Changsha, Hunan, China; Xiangya Clinical Research Center for Cancer Immunotherapy, Central South University, Changsha, Hunan, China; Research Center of Molecular Metabolomics, Xiangya Hospital, Central South University, Changsha, Hunan, China; Department of Clinical Pharmacology, Xiangya Hospital, Central South University, Changsha, Hunan, China. Electronic address: pengcongxy@csu.edu.cn.
          Article
          S0304-3835(20)30609-1
          10.1016/j.canlet.2020.11.018
          33246091
          4686da17-326a-498c-b2bb-7f0a281720f3
          History

          Agonists,Inhibitors,Long noncoding RNA,Pyruvate kinase M2,Tumor microenvironment

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