The Semaphorin 3A-AKT axis-mediated cell proliferation in salivary gland morphogenesis and adenoid cystic carcinoma pathogenesis

DOI 機関リポジトリ (HANDLE) Web Site Web Site PubMed 被引用文献4件 参考文献55件 オープンアクセス
  • 藤井, 慎介
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学 九州大学歯学発生再生（Dent-craniofacial Development and Regeneration:DDR）研究センター
  • 藤本, 龍史
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学
  • 長谷川, 佳那
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学
  • 長野, 良子
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学
  • Kari J. Kurppa
    Institute of Biomedicine and MediCity Research Laboratories, University of Turku Turku Bioscience Centre University of Turku Åbo Akademi University
  • 三上, 友理恵
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学 九州大学大学院歯学研究院口腔顎顔面病態学顎顔面腫瘍制御学
  • 田尻, 祐大
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学 九州大学大学院歯学研究院総合歯科学
  • 小倉, 萌
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学
  • 岐部, 俊郎
    国立病院機構福岡東医療センター
  • 和田, 尚久
    鹿児島大学大学院医歯学総合研究科
  • 石橋, 拓馬
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学
  • 岸田, 昭世
    鹿児島大学大学院医歯学総合研究科
  • 和田, 裕子
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学
  • 樋口, 勝規
    福岡歯科大学
  • 清島, 保
    九州大学大学院歯学研究院口腔顎顔面学口腔病理学

書誌事項

公開日
2022-08
資源種別
journal article
権利情報
  • Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
DOI
  • 10.1016/j.prp.2022.153991
公開者
Elsevier

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説明

We recently demonstrated that Semaphorin 3 A (Sema3A), the expression of which is negatively regulated by Wnt/β-catenin signaling, promotes odontogenic epithelial cell proliferation, suggesting the involvement of Sema3A in tooth germ development. Salivary glands have a similar developmental process to tooth germ development, in which reciprocal interactions between the oral epithelium and adjacent mesenchyme proceeds via stimulation with several growth factors; however, the role of Sema3A in the development of salivary glands is unknown. There may thus be a common mechanism between epithelial morphogenesis and pathogenesis; however, the role of Sema3A in salivary gland tumors is also unclear. The current study investigated the involvement of Sema3A in submandibular gland (SMG) development and its expression in adenoid cystic carcinoma (ACC) specimens. Quantitative RT-PCR and immunohistochemical analyses revealed that Sema3A was expressed both in epithelium and in mesenchyme in the initial developmental stages of SMG and their expressions were decreased during the developmental processes. Loss-of-function experiments using an inhibitor revealed that Sema3A was required for AKT activation-mediated cellular growth and formation of cleft and bud in SMG rudiment culture. In addition, Wnt/β-catenin signaling decreased the Sema3A expression in the rudiment culture. ACC arising from salivary glands frequently exhibits malignant potential. Immunohistochemical analyses of tissue specimens obtained from 10 ACC patients showed that Sema3A was hardly observed in non-tumor regions but was strongly expressed in tumor lesions, especially in myoepithelial neoplastic cells, at high frequencies where phosphorylated AKT expression was frequently detected. These results suggest that the Sema3A-AKT axis promotes cell growth, thereby contributing to morphogenesis and pathogenesis, at least in ACC, of salivary glands.

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