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HOMER3 drives oral squamous cell carcinoma progression through TRPV6 calcium influx and TUBB3 microtubule stabilization

Oncogene volume 45, pages 278–294 (2026)Cite this article

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Abstract

Oral squamous cell carcinoma (OSCC) is a highly aggressive malignancy characterized by extensive extracellular matrix (ECM) remodeling and microtubule dynamics, which drive tumor progression and therapeutic resistance. Here, we identify HOMER3 as a novel and pivotal regulator that integrates ECM stiffness and microtubule dynamics to promote OSCC malignancy. HOMER3 expression follows a distinct gradient, increasing from low levels in normal tissues to elevated levels in oral leukoplakia and highest levels in OSCC, with high expression significantly associated with advanced stages and poor survival. Mechanistically, HOMER3 acts as a scaffold protein forming two distinct functional complexes: HOMER3-CAMKK1-TRPV6, which mediates calcium influx and activates AMPK/AKT/mTOR and B-Raf/MEK/ERK pathways to promote proliferation, invasion, and ECM remodeling; and HOMER3-CAMKK1-TUBB3, which regulates microtubule dynamics and drives resistance to the chemotherapeutic agent docetaxel. Functional studies reveal that HOMER3 overexpression enhances ECM stiffness, type I collagen deposition, and Aβ accumulation in the tumor stroma, leading to tumor growth and aggressiveness, while HOMER3 knockdown reduces ECM stiffness, disrupts collagen composition, and increases sensitivity to docetaxel. These findings establish HOMER3 as a pivotal regulator of OSCC malignancy and chemoresistance, providing novel insights into its role in orchestrating the tumor microenvironment and identifying it as a promising therapeutic target for OSCC.

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Fig. 1: HOMER3 is highly expressed in OSCC and correlates with tumor progression and poor prognosis.
Fig. 2: HOMER3 regulates OSCC cell proliferation, clonogenicity, migration, and invasion.
Fig. 3: HOMER3 knockdown alters gene expression profiles and affects extracellular matrix organization and microtubule dynamics.
Fig. 4: HOMER3 regulates OSCC tumor growth in vivo.
Fig. 5: HOMER3 regulates OSCC ECM stiffness in vivo.
Fig. 6: HOMER3 modulates OSCC cell sensitivity to docetaxel by regulating microtubule dynamics.
Fig. 7: HOMER3 regulates calcium signaling, microtubule dynamics, and ECM stiffness through scaffold protein interactions.
Fig. 8: Mechanism diagram of HOMER3 in OSCC progression and chemoresistance.

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Data from the research can be accessed from the corresponding author upon reasonable request.

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Acknowledgements

This work was funded by the National Key Research and Development Program of China (2023YFC2506403 to SYS), the Key Program of National Natural Science Foundation of China (82030085 to SYS), the National Natural Science Foundation of China (82202916 to YLY), and the Innovative Research Team of High-Level Local Universities in Shanghai (SHSMU-ZLCX20212300, SSMU-ZLCX20180500). This work was also funded by Shanghai’s Top Priority Research Center (2022ZZ01017).

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  1. These authors contributed equally: Chenghui Xu, Jie Zhang.

Authors and Affiliations

  1. Department of Oral and Maxillofacial-Head Neck Oncology, Shanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University, Shanghai, China

    Chenghui Xu, Jie Zhang, Han Zhang, Lan Chen, Jinchao Zhao, Guizhu Yang, Ranran Xiao, Jiayan Zhu, Chengting Fan, Yanli Yao & Shuyang Sun

  2. National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology; Research Unit of Oral and Maxillofacial Regenerative Medicine, Chinese Academy of Medical Sciences, Shanghai, China

    Chenghui Xu, Jie Zhang, Han Zhang, Lan Chen, Jinchao Zhao, Guizhu Yang, Ranran Xiao, Jiayan Zhu, Chengting Fan, Yanli Yao & Shuyang Sun

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Contributions

SYS and YLY conceived the study and designed the experiments. CHX and JZ conducted the experiments and analyzed data. HZ, LC, JCZ, GZY, RRX, JYZ, and CTF conducted data analysis. All authors analyzed and interpreted the data, contributed to the writing of the manuscript, discussed the results and implications, and edited the manuscript at all stages. All authors read and approved the final manuscript.

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Correspondence to Yanli Yao or Shuyang Sun.

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The authors declare no competing interests.

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Approval from the Ethics Committee of the Ninth People’s Hospital, Shanghai Jiao Tong University School of Medicine, was obtained for the human tissue study, and informed consent was provided by all patients involved. All animal experimental procedures were approved by the Animal Care and Use Committee of the Affiliated Ninth People’s Hospital of Shanghai Jiao Tong University School of Medicine.

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Xu, C., Zhang, J., Zhang, H. et al. HOMER3 drives oral squamous cell carcinoma progression through TRPV6 calcium influx and TUBB3 microtubule stabilization. Oncogene 45, 278–294 (2026). https://doi.org/10.1038/s41388-025-03611-w

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