Effect of STAT3 on Lysophosphatidic Acid-Induced Oral Cancer Cell Invasion
10.17135/jdhs.2019.19.2.141
- Author:
Zi Hae SONG
1
;
Kyung Hwa CHO
;
Jin Young KIM
;
Hoi Young LEE
Author Information
1. Department of Pharmacology, College of Medicine, Konyang University, Daejeon 35365, Korea. metaandy@naver.com
- Publication Type:Original Article
- Keywords:
Epithelial-mesenchymal transition;
Lysophospholipids;
Mouth neoplasms;
STAT3 transcription factor
- MeSH:
Cell Survival;
Epithelial-Mesenchymal Transition;
Gene Expression;
Humans;
Immunoblotting;
In Vitro Techniques;
Incidence;
Lysophospholipids;
Mammals;
Mouth Neoplasms;
Neoplasm Metastasis;
Phosphorylation;
Smoke;
Smoking;
STAT3 Transcription Factor;
Survival Rate;
Transcription Factors;
Transducers
- From:
Journal of Dental Hygiene Science
2019;19(2):141-146
- CountryRepublic of Korea
- Language:English
-
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.
