Effect of STAT3 on Lysophosphatidic Acid-Induced Oral Cancer Cell Invasion
Song Zi-Hae, 조경화, 김진영, 이회영,
소속 상세정보
( Song Zi-Hae ) - Konyang University College of Medicine Department of Pharmacology
조경화 ( Cho Kyung-Hwa ) - Konyang University College of Medicine Department of Pharmacology
김진영 ( Kim Jin-Young ) - Konyang University College of Medicine Department of Pharmacology
이회영 ( Lee Hoi-Young ) - Konyang University College of Medicine Department of Pharmacology
Abstract
Background: Oral cancer has a high incidence worldwide and has been closely associated with smoking, alcohol, and infection by the human papillomavirus. Metastasis is highly important for oral cancer survival. Lysophosphatidic acid (LPA) is a bioactive lipid mediator that promotes various cellular processes, including cell survival, proliferation, metastasis, and invasion. Signal transducer and activator of transcription (STATs) are transcription factors that mediate gene expression. Among the seven types of STATs in mammals, STAT3 is involved in invasion and metastasis of numerous tumors. However, little is known about the role of STAT3 in oral tumor invasion. In the present study, we hypothesized that STAT3 mediates LPA-induced oral cancer invasion.
Methods: Immunoblotting was performed to analyze LPA-induced STAT3 activation. 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay was performed to assess the survival rates of YD-10B cells. STAT3 levels in LPA-treated oral tumor cells were evaluated by performing in vitro invasion assay.
Results: To the best of our knowledge, this is the first study to demonstrate that LPA enhances STAT3 phosphorylation in oral cancer. In addition, treatment with WP1066, a selective inhibitor of STAT3, at a concentration that does not cause severe reduction in cell viability, significantly attenuated LPA-induced YD-10B cancer cell invasion.
Conclusion: The results suggested that LPA induces oral tumor cells with greater invasive potential via STAT3 activation. Our findings provided important insights into the mechanisms underlying mouth neoplasms.
키워드
Epithelial-mesenchymal transition; Lysophospholipids; Mouth neoplasms; STAT3 transcription factor
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