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Oncology Letters
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Print ISSN: 1792-1074 Online ISSN: 1792-1082
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December-2026 Volume 32 Issue 6

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Article Open Access

PEG10/TRIB3 axis is associated with malignant behavior and Notch‑related signaling in oral squamous cell carcinoma cells

  • Authors:
    • Jing Zhang
    • Ying Liu
  • View Affiliations / Copyright

    Affiliations: Department of Endodontics, Stomatological Hospital, School of Stomatology, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 560
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    Published online on: October 22, 2026
       https://doi.org/10.3892/ol.2026.15914
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Abstract

Oral squamous cell carcinoma (OSCC) is an aggressive oral epithelial neoplasm for which the expression of paternally expressed gene 10 (PEG10) has notable prognostic implications. However, the functional role of this protein in OSCC remains to be fully elucidated. The present study aimed to explore the function of PEG10 in regulating OSCC cell behavior and the potential mechanisms of this regulation. Cell Counting Kit‑8, 5‑ethynyl‑2'‑deoxyuridine, wound healing and Transwell assays were employed to estimate cell proliferation, migration and invasion, respectively. Furthermore, flow cytometry assays were used to detect the cell cycle status and apoptosis of OSCC cells. Western blot analysis was used to examine the expression of PEG10 and Tribbles pseudokinase 3 (TRIB3), as well as cell cycle‑, apoptosis‑ and Notch signaling‑associated proteins. The HDOCK server (a hybrid docking server for protein and nucleic acid complex prediction) and co‑immunoprecipitation assays were employed to investigate the relationship between PEG10 and TRIB3. The present study found PEG10 to be highly expressed in OSCC tissues and cells. PEG10 knockdown reduced cell proliferation, migration and invasion, arrested the cell cycle in the G0/G1 phase and stimulated apoptosis. TRIB3 expression was also shown to be elevated in OSCC cells and was decreased following PEG10 knockdown. Concurrent TRIB3 overexpression partially reversed the effects of PEG10 knockdown on malignant phenotypes and Notch‑related protein expression. These findings suggested that the PEG10/TRIB3 axis may be associated with malignant behavior and Notch‑related signaling in OSCC.

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Copy and paste a formatted citation
Spandidos Publications style
Zhang J and Liu Y: <em>PEG10/TRIB3</em> axis is associated with malignant behavior and Notch‑related signaling in oral squamous cell carcinoma cells. Oncol Lett 32: 560, 2026.
APA
Zhang, J., & Liu, Y. (2026). <em>PEG10/TRIB3</em> axis is associated with malignant behavior and Notch‑related signaling in oral squamous cell carcinoma cells. Oncology Letters, 32, 560. https://doi.org/10.3892/ol.2026.15914
MLA
Zhang, J., Liu, Y."<em>PEG10/TRIB3</em> axis is associated with malignant behavior and Notch‑related signaling in oral squamous cell carcinoma cells". Oncology Letters 32.6 (2026): 560.
Chicago
Zhang, J., Liu, Y."<em>PEG10/TRIB3</em> axis is associated with malignant behavior and Notch‑related signaling in oral squamous cell carcinoma cells". Oncology Letters 32, no. 6 (2026): 560. https://doi.org/10.3892/ol.2026.15914
Copy and paste a formatted citation
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Spandidos Publications style
Zhang J and Liu Y: <em>PEG10/TRIB3</em> axis is associated with malignant behavior and Notch‑related signaling in oral squamous cell carcinoma cells. Oncol Lett 32: 560, 2026.
APA
Zhang, J., & Liu, Y. (2026). <em>PEG10/TRIB3</em> axis is associated with malignant behavior and Notch‑related signaling in oral squamous cell carcinoma cells. Oncology Letters, 32, 560. https://doi.org/10.3892/ol.2026.15914
MLA
Zhang, J., Liu, Y."<em>PEG10/TRIB3</em> axis is associated with malignant behavior and Notch‑related signaling in oral squamous cell carcinoma cells". Oncology Letters 32.6 (2026): 560.
Chicago
Zhang, J., Liu, Y."<em>PEG10/TRIB3</em> axis is associated with malignant behavior and Notch‑related signaling in oral squamous cell carcinoma cells". Oncology Letters 32, no. 6 (2026): 560. https://doi.org/10.3892/ol.2026.15914
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