간행물
International Journal of Oral Biology KCI 등재
- 발행기관 대한구강생물학회
- 자료유형 학술지
- 간기 계간
- ISSN 1226-7155 (Print)2287-6618 (Online)
- 수록기간 1977 ~ 2026
- 주제분류 의약학 > 치의학 의약학 분류의 다른 간행물
- 십진분류KDC 515DDC 610
권호리스트/논문검색
Vol.51 No.1 (2026년 3월) 1건
1.
2026.03
구독 인증기관 무료, 개인회원 유료
Epithelial-mesenchymal transition (EMT) is a critical process that drives tumor invasion and metastasis in oral squamous cell carcinoma (OSCC). Although transforming growth factor beta 1 (TGF-β1) and epidermal growth factor (EGF) are well-established inducers of EMT, the signaling crosstalk underlying their combined effects during the initial phase remains poorly defined. This study investigated the impact of combined TGF-β1 and EGF stimulation on EMTrelated phenotypic and molecular changes in HSC-3 OSCC cells. The cells were treated with TGF-β1 (10 ng/mL) and EGF (100 ng/mL), either individually or in combination. Cell proliferation, morphological changes, EMT marker expression, signaling pathway activation, and migratory capacity were assessed using cell counting kit-8 assays, quantitative morphological analysis, RT-qPCR, immunoblotting, and wound healing assays, respectively. Although TGF-β1 or EGF alone induced partial EMT-like changes, combined stimulation produced a pronounced spindleshaped morphology, an increased cell aspect ratio, and loss of epithelial cell-cell contact. Consistently, cotreatment led to greater repression of E-cadherin and enhanced upregulation of N-cadherin and Vimentin compared with single treatments. Notably, dual exposure markedly increased Smad2 and extracellular signal-regulated kinase (ERK) phosphorylation while accelerating cell migration. These findings indicate that TGF-β1 and EGF cooperatively promote EMT and migratory behavior through the coordinated activation of Smad2 and MAPK/ERK signaling pathways, highlighting this crosstalk as a potential therapeutic target for OSCC metastasis.
4,000원
