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<p>This study investigated the role of pyruvate kinase M2 (PKM2) in the progression of nasopharyngeal carcinoma (NPC) and in the regulation of NPC cell survival and apoptosis. PKM2 expression was markedly elevated in 30 NPC samples and NPC cell lines compared to that in nasopharyngeal NP69 cells and adjacent healthy tissues. Functional loss- and gain-of-function experiments were conducted to evaluate the role and underlying mechanisms of PKM2. Cell proliferation was evaluated using colony formation and CCK-8 assays, whereas apoptosis was quantified by Annexin V/PI flow cytometry (FCM). Oxidative stress biomarkers were examined to assess redox homeostasis in NPC cells. Silencing rather than overexpression of PKM2 was found to inhibit NPC cell proliferation and colony formation, while enhancing apoptosis. Additionally, the Nrf2/HO-1/GSH signaling pathway was inhibited following silencing of PKM2. Administration of the Nrf2 activator bardoxolone methyl (Bar) counteracted the suppressive effect of PKM2 silencing on NPC cell survival and apoptosis. In vivo tumorigenesis experiments showed that PKM2 knockdown reduced the growth rate of NPC. In conclusion, these findings highlight PKM2 as a potential therapeutic target in NPC due to its role in regulating the Nrf2/HO-1 axis.</p>

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PKM2 Deficiency Results in Reduced Proliferation of Nasopharyngeal Carcinoma Cells by Deactivation of Nrf2-HO-1-GSH Signaling

  • 期刊论文

  • 发表日期：

    2026年3月13日

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  • Rui Liu,
  • Minghui Zhou,
  • Puwen Zhang

摘要

This study investigated the role of pyruvate kinase M2 (PKM2) in the progression of nasopharyngeal carcinoma (NPC) and in the regulation of NPC cell survival and apoptosis. PKM2 expression was markedly elevated in 30 NPC samples and NPC cell lines compared to that in nasopharyngeal NP69 cells and adjacent healthy tissues. Functional loss- and gain-of-function experiments were conducted to evaluate the role and underlying mechanisms of PKM2. Cell proliferation was evaluated using colony formation and CCK-8 assays, whereas apoptosis was quantified by Annexin V/PI flow cytometry (FCM). Oxidative stress biomarkers were examined to assess redox homeostasis in NPC cells. Silencing rather than overexpression of PKM2 was found to inhibit NPC cell proliferation and colony formation, while enhancing apoptosis. Additionally, the Nrf2/HO-1/GSH signaling pathway was inhibited following silencing of PKM2. Administration of the Nrf2 activator bardoxolone methyl (Bar) counteracted the suppressive effect of PKM2 silencing on NPC cell survival and apoptosis. In vivo tumorigenesis experiments showed that PKM2 knockdown reduced the growth rate of NPC. In conclusion, these findings highlight PKM2 as a potential therapeutic target in NPC due to its role in regulating the Nrf2/HO-1 axis.