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ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling

  • Authors:
    • Ying Liu
    • Yinyin Hou
    • Fan Zhang
    • Xifang Wang
  • View Affiliations / Copyright

    Affiliations: Department of Medical Oncology, Shaanxi Provincial People's Hospital, Xi'an, Shaanxi 710068, P.R. China
    Copyright: © Liu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 127
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    Published online on: February 5, 2024
       https://doi.org/10.3892/etm.2024.12415
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Abstract

Colorectal cancer (CRC) is one of the most prevailing and lethal forms of cancer globally. α‑enolase (ENO1) has been well documented to be involved in the progression and drug resistance of CRC. The present study was designed to specify the role of ENO1 in major events during the process of CRC and to introduce its latent functional mechanism. ENO1 expression was determined by western blot analysis. Extracellular acidification rates were assessed using an XF96 extracellular flux analyzer. Glucose uptake, lactic acid production, total iron levels and ferroptosis‑related markers were examined with corresponding kits. A dichlorodihydrofluorescein diacetate probe measured intracellular reactive oxygen species content. Western blotting detected the expression of glycolysis‑ and ferroptosis‑related proteins. CCK‑8 and EdU staining assays assessed cell proliferation. In the current study, ENO1 was highly expressed in CRC cells. Knockdown of ENO1 markedly reduced the glycolysis and accelerated the ferroptosis in CRC cells. Moreover, the inhibitory effects of WZB117, a specific inhibitor of glycolysis‑related glucose transporter type 1, on CRC cell proliferation were further enhanced by ENO1 interference. In addition, silencing of ENO1 inactivated the AKT/STAT3 signaling. The AKT activator SC79 partially reversed the effects of ENO1 deficiency on the AKT/STAT3 signaling, glycolysis, proliferation as well as ferroptosis in CRC cells. In summary, inactivation of AKT/STAT3 signaling mediated by ENO1 inhibition might boost the ferroptosis and suppress the glycolysis in CRC cells.
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Copy and paste a formatted citation
Spandidos Publications style
Liu Y, Hou Y, Zhang F and Wang X: ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling. Exp Ther Med 27: 127, 2024.
APA
Liu, Y., Hou, Y., Zhang, F., & Wang, X. (2024). ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling. Experimental and Therapeutic Medicine, 27, 127. https://doi.org/10.3892/etm.2024.12415
MLA
Liu, Y., Hou, Y., Zhang, F., Wang, X."ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling". Experimental and Therapeutic Medicine 27.4 (2024): 127.
Chicago
Liu, Y., Hou, Y., Zhang, F., Wang, X."ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling". Experimental and Therapeutic Medicine 27, no. 4 (2024): 127. https://doi.org/10.3892/etm.2024.12415
Copy and paste a formatted citation
x
Spandidos Publications style
Liu Y, Hou Y, Zhang F and Wang X: ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling. Exp Ther Med 27: 127, 2024.
APA
Liu, Y., Hou, Y., Zhang, F., & Wang, X. (2024). ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling. Experimental and Therapeutic Medicine, 27, 127. https://doi.org/10.3892/etm.2024.12415
MLA
Liu, Y., Hou, Y., Zhang, F., Wang, X."ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling". Experimental and Therapeutic Medicine 27.4 (2024): 127.
Chicago
Liu, Y., Hou, Y., Zhang, F., Wang, X."ENO1 deletion potentiates ferroptosis and decreases glycolysis in colorectal cancer cells via AKT/STAT3 signaling". Experimental and Therapeutic Medicine 27, no. 4 (2024): 127. https://doi.org/10.3892/etm.2024.12415
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