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Review
. 2024 Oct 4:15:1480701.
doi: 10.3389/fimmu.2024.1480701. eCollection 2024.

TEAD transcription factor family emerges as a promising therapeutic target for oral squamous cell carcinoma

Affiliations
Review

TEAD transcription factor family emerges as a promising therapeutic target for oral squamous cell carcinoma

Shuang Wang et al. Front Immunol. .

Abstract

The treatment of oral squamous cell carcinoma (OSCC) remains a significant difficulty, as there has been no improvement in survival rates over the past fifty years. Hence, exploration and confirmation of new dependable treatment targets and biomarkers is imperative for OSCC therapy. TEAD transcription factors are crucial for integrating and coordinating multiple signaling pathways that are essential for embryonic development, organ formation, and tissue homeostasis. In addition, by attaching to coactivators, TEAD modifies the expression of genes such as Cyr61, Myc, and connective tissue growth factor, hence facilitating tumor progression. Therefore, TEAD is regarded as an effective predictive biomarker due to its significant connection with clinical parameters in several malignant tumors, including OSCC. The efficacy of existing drugs that specifically target TEAD has demonstrated encouraging outcomes, indicating its potential as an optimal target for OSCC treatment. This review provides an overview of current targeted therapy strategies for OSCC by highlighting the transcription mechanism and involvement of TEAD in oncogenic signaling pathways. Finally, the feasibility of utilizing TEAD as an innovative approach to address OSCC and its potential clinical applications were analyzed and discussed.

Keywords: TEA domain transcription factors; biomarkers; hippo signaling pathway; molecular targeted therapy; oral squamous cell carcinoma.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Protein structure of the TEAD family in the human protein atlas. (A) TEAD1 protein structure; (B) TEAD2 protein structure; (C) TEAD3 protein structure; (D) TEAD4 protein structure.
Figure 2
Figure 2
mRNA expression of the TEAD family in cancer in the human protein atlas (mRNA data from the TCGA database). (A) TEAD1 mRNA expression; (B) TEAD2 mRNA expression; (C) TEAD3 mRNA expression; (D) TEAD4 mRNA expression.
Figure 3
Figure 3
Immunohistochemical staining of TEAD3 and TEAD4 in HNSCC tissues in the human protein atlas. (A) positive expression of TEAD3 in HNSCC tissues; (B) positive expression of TEAD4 in HNSCC tissues; Scale bars =200 μm.

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References

    1. Luo M, Xu Y, Chen H, Wu Y, Pang A, Hu J, et al. . Advances of targeting the YAP/TAZ-TEAD complex in the hippo pathway for the treatment of cancers. Eur J Med Chem. (2022) 244:114847. doi: 10.1016/j.ejmech.2022.114847 - DOI - PubMed
    1. da Silva EZM, Fraga-Silva TFC, Yuan Y, Alves MG, Publio GA, da Fonseca CK, et al. . Kallikrein 5 inhibition by the lympho-epithelial kazal-type related inhibitor hinders matriptase-dependent carcinogenesis. Cancers (Basel). (2021) 13:4395. doi: 10.3390/cancers13174395 - DOI - PMC - PubMed
    1. Chien C-Y, Chen YC, Hsu CC, Chou YT, Shiah SG, Liu SY, et al. . YAP-dependent BiP induction is involved in nicotine-mediated oral cancer Malignancy. Cells. (2021) 10:2080. doi: 10.3390/cells10082080 - DOI - PMC - PubMed
    1. Choi W, Kim J, Park J, Lee Dh, Hwang D, Kim Jh, et al. . YAP/TAZ initiates gastric tumorigenesis via upregulation of MYC. Cancer Res. (2018) 78:3306. doi: 10.1158/0008-5472.CAN-17-3487 - DOI - PubMed
    1. Chen X, Gu W, Wang Q, Fu X, Wang Y, Xu X, et al. . C-MYC and BCL-2 mediate YAP-regulated tumorigenesis in OSCC. Oncotarget. (2018) 9:668. doi: 10.18632/oncotarget.23089 - DOI - PMC - PubMed

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Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The Qingdao University Medical Group Research Project (2022-44, YLJT20231001) provided financial support for this work.

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