國家衛生研究院 NHRI:Item 3990099045/14371
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/14371


    Title: Mitochondrial phosphoenolpyruvate carboxykinase promotes tumor growth in estrogen receptor-positive breast cancer via regulation of the mTOR pathway
    Authors: Hsu, HP;Chu, PY;Chang, TM;Huang, KW;Hung, WC;Jiang, SS;Lin, HY;Tsai, HJ
    Contributors: National Institute of Cancer Research
    Abstract: BACKGROUND: Tumor cells may aberrantly express metabolic enzymes to adapt to their environment for survival and growth. Targeting cancer-specific metabolic enzymes is a potential therapeutic strategy. Phosphoenolpyruvate carboxykinase (PEPCK) catalyzes the conversion of oxaloacetate to phosphoenolpyruvate and links the tricarboxylic acid cycle and glycolysis/gluconeogenesis. Mitochondrial PEPCK (PEPCK-M), encoded by PCK2, is an isozyme of PEPCK and is distributed in mitochondria. Overexpression of PCK2 has been identified in many human cancers and demonstrated to be important for the survival program initiated upon metabolic stress in cancer cells. We evaluated the expression status of PEPCK-M and investigated the function of PEPCK-M in breast cancer. METHODS: We checked the expression status of PEPCK-M in breast cancer samples by immunohistochemical staining. We knocked down or overexpressed PCK2 in breast cancer cell lines to investigate the function of PEPCK-M in breast cancer. RESULTS: PEPCK-M was highly expressed in estrogen receptor-positive (ER(+) ) breast cancers. Decreased cell proliferation and G(0) /G(1) arrest were induced in ER(+) breast cancer cell lines by knockdown of PCK2. PEPCK-M promoted the activation of mTORC1 downstream signaling molecules and the E2F1 pathways in ER(+) breast cancer. In addition, glucose uptake, intracellular glutamine levels, and mTORC1 pathways activation by glucose and glutamine in ER(+) breast cancer were attenuated by PCK2 knockdown. CONCLUSION: PEPCK-M promotes proliferation and cell cycle progression in ER(+) breast cancer via upregulation of the mTORC1 and E2F1 pathways. PCK2 also regulates nutrient status-dependent mTORC1 pathway activation in ER(+) breast cancer. Further studies are warranted to understand whether PEPCK-M is a potential therapeutic target for ER(+) breast cancer.
    Date: 2023-01
    Relation: Cancer Medicine. 2023 Jan;12(2):1588-1601.
    Link to: http://dx.doi.org/10.1002/cam4.4969
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2045-7634&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000815811200001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85132722575
    Appears in Collections:[Hui-Jen Tsai] Periodical Articles
    [Shih-Sheng Jiang] Periodical Articles
    [Wen-Chun Hung] Periodical Articles

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