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Article

Depletion of PHLDB2 Suppresses Epithelial–Mesenchymal Transition and Enhances Anti-Tumor Immunity in Head and Neck Squamous Cell Carcinoma

1
Department of Oral and Maxillofacial Surgery, Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, 56 Lingyuan Road West, Guangzhou 510055, China
2
Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510080, China
3
Guanghua School of Stomatology, Sun Yat-sen University, Guangzhou 510055, China
4
Department of Stomatology, The Fifth Affiliated Hospital, Sun Yat-sen University, Zhuhai 519000, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Biomolecules 2024, 14(2), 232; https://doi.org/10.3390/biom14020232
Submission received: 8 January 2024 / Revised: 6 February 2024 / Accepted: 15 February 2024 / Published: 17 February 2024
(This article belongs to the Special Issue Biomarkers in Oral Diseases 2.0)

Abstract

The role of Pleckstrin homology-like domain family B member 2 (PHLDB2) in the regulation of cell migration has been extensively studied. However, the exploration of PHLDB2 in head and neck squamous cell carcinoma (HNSCC) is still limited in terms of expression, function, and therapeutic potential. In this study, we discovered an upregulation of PHLDB2 expression in HNSCC tissues which was correlated with a negative prognosis in patients with HNSCC. Additionally, we determined that a high level of expression of PHLDB2 is crucial for maintaining cell migration through the regulation of the epithelial–mesenchymal transition (EMT). Furthermore, we demonstrated that the ablation of PHLDB2 in tumor cells inhibited tumorigenicity in a C3H syngeneic tumor-bearing mouse model. Mechanistically, PHLDB2 was found to be involved in the regulation of T cell anti-tumor immunity, primarily by enhancing the activation and infiltration of CD8+ T cells. In light of these findings, PHLDB2 emerges as a promising biomarker and therapeutic target for interventions in HNSCC.
Keywords: anti-tumor immunity; CD8+T; epithelial–mesenchymal transition; head and neck squamous cell carcinoma; PHLDB2 anti-tumor immunity; CD8+T; epithelial–mesenchymal transition; head and neck squamous cell carcinoma; PHLDB2

Share and Cite

MDPI and ACS Style

Li, H.; Wang, Z.; Liang, H.; Liu, X.; Liu, H.; Zhuang, Z.; Hou, J. Depletion of PHLDB2 Suppresses Epithelial–Mesenchymal Transition and Enhances Anti-Tumor Immunity in Head and Neck Squamous Cell Carcinoma. Biomolecules 2024, 14, 232. https://doi.org/10.3390/biom14020232

AMA Style

Li H, Wang Z, Liang H, Liu X, Liu H, Zhuang Z, Hou J. Depletion of PHLDB2 Suppresses Epithelial–Mesenchymal Transition and Enhances Anti-Tumor Immunity in Head and Neck Squamous Cell Carcinoma. Biomolecules. 2024; 14(2):232. https://doi.org/10.3390/biom14020232

Chicago/Turabian Style

Li, Hongyu, Ziyi Wang, Huiting Liang, Xiaoyong Liu, Haichao Liu, Zehang Zhuang, and Jinsong Hou. 2024. "Depletion of PHLDB2 Suppresses Epithelial–Mesenchymal Transition and Enhances Anti-Tumor Immunity in Head and Neck Squamous Cell Carcinoma" Biomolecules 14, no. 2: 232. https://doi.org/10.3390/biom14020232

APA Style

Li, H., Wang, Z., Liang, H., Liu, X., Liu, H., Zhuang, Z., & Hou, J. (2024). Depletion of PHLDB2 Suppresses Epithelial–Mesenchymal Transition and Enhances Anti-Tumor Immunity in Head and Neck Squamous Cell Carcinoma. Biomolecules, 14(2), 232. https://doi.org/10.3390/biom14020232

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