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Demethoxycurcumin suppresses HK2-mediated glycolysis by targeting PTEN/Akt signaling

Cancer Gene Therapy (2025)Cite this article

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Abstract

Aerobic glycolysis is a hallmark of tumor cells, with the expression of glycolytic enzymes often being upregulated in many cancers, leading to enhanced metabolic activity. Among the key rate-limiting enzymes in this process, Hexokinase 2 (HK2) plays a crucial role in sustaining the biological activities of human cancers. Therefore, HK2 is considered a potential therapeutic target, although effective targeted drugs for oral squamous cell carcinoma (OSCC) treatment are currently lacking. To confirm potent anti-tumor agents that inhibit HK2 expression, we screened a library of 639 natural products and discovered that Demethoxycurcumin (Deme) was the most effective anti-tumor agent via inhibiting HK2-mediated glycolysis in OSCC cells, inducing intrinsic apoptosis. Mechanistically, Deme enhanced the interaction between USP13 and PTEN, leading to the stabilization of PTEN and consequent downregulation of HK2 via the PTEN/Akt/HK2 pathway. Notably, HK2 overexpression reversed the inhibitory effect of Deme on OSCC cells. Furthermore, at the tumor-inhibitory dose, Deme showed no effect on non-tumor HaCat cells. In vivo, Deme significantly suppressed tumor growth without apparent toxicity to vital organs. Together, these data suggest that Deme is a promising and safe anti-tumor compound that downregulates HK2 expression, providing a potential therapeutic strategy for OSCC treatment.

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Fig. 1: HK2 maintains the tumorigenic potential of oral squamous cell carcinoma (OSCC) cells.
Fig. 2: HK2 deficiency delays the tumor growth of OSCC cells in vivo.
Fig. 3: Demethoxycurcumin (Deme) inhibits glycolysis in OSCC.
Fig. 4: Deme reduces HK2 protein levels and triggers intrinsic apoptosis.
Fig. 5: Deme modulates the PTEN/Akt/HK2 signaling pathway.
Fig. 6: Deme enhances PTEN deubiquitination.
Fig. 7: Knockout of USP13 can reverse the inhibitory effect of Deme on OSCC cells.
Fig. 8: Deme inhibits tumor growth in vivo.

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Data sharing not applicable to this article as no datasets were generated or analyzed during the current study.

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Funding

This work was supported by Hunan Natural Science Foundation Outstanding Youth Fund [grant numbers 2023JJ10091]; Wisdom Accumulation and Talent Cultivation Project of the Third Xiangya Hospital of Central South University [grant number BJ202203]; Research Project of Teaching Reform in Colleges and Universities of Hunan Province [HNJG-20230110]; and Education and Teaching Reform Research Project of Central South University [2023jy200].

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  1. These authors contributed equally: Jinzhuang Liao, Shiming Tan.

Authors and Affiliations

  1. Department of Radiology, The Third Xiangya Hospital of Central South University, Changsha, Hunan, China

    Jinzhuang Liao, Shiming Tan, Shuangze Han, Ruirui Wang, Pengfei Guo, Wei Zheng & Wei Li

  2. Department of Interventional Therapy, National Cancer Center/National Clinical Research Center for Cancer/Cancer Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China

    Jinzhuang Liao

  3. Department of Hematology, The Third Xiangya Hospital, Central South University, Changsha, Hunan, China

    Shiming Tan

  4. Department of Ultrasound, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China

    Shuangze Han

  5. Key Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Xiangya Hospital, Central South University, Changsha, China

    Xinfang Yu

  6. Key Laboratory of Carcinogenesis of National Health Commission, Cancer Research Institute and School of Basic Medical Science, Xiangya School of Medicine, Central South University, Changsha, China

    Xinfang Yu

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  1. Jinzhuang Liao
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Contributions

JZL: Data curation, methodology, formal analysis, writing original draft, writing–review and editing, visualization, project administration. SMT: Writing–review and editing, visualization, data curation, Formal analysis, methodology, project administration. SZH, RRW, PFG: Formal analysis, methodology, project administration. ZW: Fundings, methodology. XFY: Methodology, visualization, and supervision. WL: Fundings, writing–review and editing, conceptualization, and supervision. All Authors have read and agreed to the published version of the manuscript.

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Correspondence to Wei Li.

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All animal experiments were approved by the Institutional Animal Care and Use Committee, the Third Xiangya Hospital of Central South University (Changsha, China). All methods were performed in accordance with the relevant guidelines and regulations. Clinical trial number: not applicable.

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Liao, J., Tan, S., Han, S. et al. Demethoxycurcumin suppresses HK2-mediated glycolysis by targeting PTEN/Akt signaling. Cancer Gene Ther (2025). https://doi.org/10.1038/s41417-025-00972-y

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