Adherent cells, such as those found in epithelial tissues, must be physically associated with extracellular matrix (ECM)components to survive. Though stimulation by growth factors is an essential factor in cell survival, normal cells also requires cell adhesion to ECM proteins. The cessation of these anchorage-mediated signals seems to be a common mechanism to physiolog ically t erminate t he l ife cycle of t hese c ells b y apoptosis. This form o f cell death has been termed anoikis.In cancer, resistance to anoikis of cancer cell is important in invasion and metastasis. The present study investigated the intracellular mechanism involved in anoikis, especially in cells treated with epigallocatechin- 3-gallate(EGCG). To induce anoikis, cell culture plates were coated with 10 ㎍/ml poly-HEMA. A549 lung adenocarcinoma cells were grown in RPMI 1640 medium with/without 10% fetal bovine serum, and then cells were replated on cell culture dishes coated with poly-HEMA in the presence or absence of serum. On the other hand, EGFR inhibitor, PI3K inhibitor, and EGCG were treated to the anoikis status cells, in order to evaluate the factors of anoikis. The result revealed that growth factors or loss of adhesion can increase phosphorylate Akt. In addition, lack of cell adhesion fails to activate pro-apoptotic factors directly. Activity of Erk kinase depends on not only EGFR signaling but also cell adhesion. Akt activation is mainly affected by EGCG whereas Raf-1 activation is controlled by the presence of cell contact. In addition, EGCG increased the level of NFkB, whereas phophroylated PTEN and total PTEN were not different. In this report,increase of NFkB was correlated with Akt phosphorylation, suggesting that EGCG can protect cells from detachment–induced cell death through Akt activation and subsequent NFkB

I. INTRODUCTION
 II. MATERIALS AND METHODS
  1. Cell culture
  2. Chemicals
  3. Suspension culture
  4. Western Blot Analysis
 III. RESULTS
  1. Either growth factors or adhesion canphosphorylate Akt
  2. Lack of cell adhesion fails to activatepro-apoptotic factors directly
  3. Activity of E rk k inase depends on not onlyEGFR signaling but also cell adhesion
  4. Akt activation is mainly affected by EGCGwhereas Raf-1 activation is controlled bythe presence of cell contact
 
IV. DISCUSSION
 V. REFERENCES

• 박형목(Department of Oral Pathology) | Hyung Mok Park
• 이창식(Department of Oral Pathology) | Chang Sik Lee
• 정진(Department of Oral Microbiology) | Jin Chung
• 박봉수(Department of Oral Anatomy, School of Dentistry, Pusan National University) | Bong Soo Park
• 유미현(Department of Oral Pathology) | Mi Heon Ryu
• 박혜련(Department of Oral Pathology) | Hae Ryoun Park correspondence