논문 상세보기

Epigallocatechin-3-gallate(EGCG)이 구강 편평세포암종 세포사를 유발하는 기전 연구 KCI 등재

Epigallocatechin-3-gallate (EGCG) Induces Cell Death of Oral Squamous

  • 언어ENG
  • URLhttps://db.koreascholar.com/Article/Detail/292944
구독 기관 인증 시 무료 이용이 가능합니다. 4,000원
대한구강악안면병리학회지 (The Korean Journal of Oral and Maxillofacial Pathology)
대한구강악안면병리학회 (Korean Academy Of Oral And Maxillofacial Pathology)
초록

Green tea, derived from the plant Camellia sinensis, is one of the most common beverages consumed worldwide. Epigallocatechin-3-gallate (EGCG) is the most abundant and bioactive polyphenolic constituent in green tea. Understanding how intracellular signaling pathways respond to EGCG may provide a clue to the difference of cell responses and basis for usefulness of EGCG as a chemopreventive and/or chemotherapeutic agent. In the present study, we tried to check whether EGCG could be a useful agent in chemotherapeutic treatment of oral squamous carcinoma. Furthermore, we investigated which signaling pathway is involved in biologic activities of EGCG. EGCG induced the cell death of oral squamous carcinoma cells. Furthermore, it increased phosphorylation of Akt in serum-strarved oral squamous carcinoma cells. But, initial increase of Akt activation did not affect cell survival. Activities of Raf-1 and Erk showed inconsistent response to EGCG treatment, but Erk phosphorylation is consistent with Raf-1 activity in YD 10B cells. These changes of Raf-1 and Erk activity in EGCG treated cells were different depending on cell line type. Supposedly, the difference of cell component may affect the Raf-1 and Erk reactivity to EGCG treatment. Akt activation by EGCG is independent on activities of PDK1 and PTEN, and expression of bax and bcl-2 proteins were not changed by EGCG treatment. Therefore, EGCG treatment did not induce the apoptosis of YD 10B cell. On the other hand, vascular adhesion molecule (VCAM) was decreased by EGCG treatment, so it is possible that decrease of VCAM can play certain role in survival and/or cell death in EGCG treated cells

목차
I. INTRODUCTION
 II. MATERIALS AND METHODS
  1. Cell culture
  2. EGCG treatments
  3. MTT assay
  4. Western Blot Analysis
 III. RESULTS
  1. EGCG induced death of oral squamouscarcinoma cells
  2. EGCG increased phosphorylation of Aktin serum-starved oral squmaous carcinomacells
  3. Akt activation by EGCG was independenton activities of PDK1 and PTEN
  4. Activities of Raf-1 and Erk showed inconsistentresponse to EGCG treatment,but Erk phosphorylation is concordantwith Raf-1 activity in YD 10B cells
  5. Expressionsof bax and bcl-2 proteinswere not changed by EGCG treatment
  6. Vascular cell adhesion molecule wassignificantlydecreased by EGCG treatmentin YD 10B cells
 IV. DISCUSSION
 V. REFERENCES
저자
  • 박형목(Department of Oral Pathology) | Hyung Mok Park
  • 이은경(Department of Oral Pathology) | Eun Kyoung Lee
  • 정진(Department of Oral Microbiology) | Jin Chung
  • 박봉수(Department of Oral Anatomy, School of Dentistry, Pusan National University) | Bong Soo Park
  • 박혜련(Department of Oral Pathology) | Hae Ryoun Park
  • 유미현(Department of Oral Pathology) | Mi Heon Ryu correspondence