Cinnamaldehyde is known to have the antitumor effects in vitro and in vivo. In this study, we showed a potent and irreversible cytotoxic activity of the Cinnamaldehyde derivative 2'-benzoyloxycinnamaldehyde (BCA) in human Squamous oral cell carcinoma cell, YD-10B. BCA induced YD-10B cell apoptosis in a dose-responsive manner. BCA-induced apoptosis was associated with corresponding increases in a series of key components in the mitochondria-mediated apoptosis pathways, followed by caspase cleavage and PARP activation. We also observed that BCA induced autophagy through Akt/mTOR pathway in YD-10B cells. BCA treatment increased LC3B-II expression, and induced the formation of autophagosomes and autophagic vacuoles. These experimental findings suggest that BCA is a potent inhibitor of cell proliferation in YD-10B cells and provide new insights about leading to the possible development of a new therapeutic agent.

Odontoblasts and/or dental pulp cells are responsible for tooth repair as well as dentin formation. Adhesion and migration are critical processes for tissue regeneration. This study was performed to clarify whether Pam3 modulates adhesion and migration of a murine odontoblast-like cell line, MDPC-23 cell and TLR2 signaling is engaged in this process. TLR2 expression in MDPC-23 cells was examined by RT-PCR. Adhesion assay was performed using type Ⅰ collagen-coated plates. Migration ability was determined by a commercial assay kit. Phosphorylation of IκB-α, JNK, p38, and ERK was examined by Western blot analysis. TLR2 was functionally expressed in MDPC-23 cells. Pam3CSK treatment enhanced adhesion and migration of MDPC-23 cells in a dose-dependent manner. Blockade of TLR2 using its antibody restored Pam3CSK-induced adhesion and migration of MDPC-23 cells. These findings indicate that Pam3CSK, an immune activator from gram negative bacteria, can promote adhesion and migration ability of MDPC-23 cells via TLR2.

Hereditary dentin defects consists of dentin dysplasia(DD) and denti nogenesis imperfecta(Dr) ‘ The Dl associated with osteogenesis imperfecta has been classified as DI type 1. whereas isolated inherited defects have been categori zed as DI types II and III , However‘ whether DI type III should be considered a distinct phenotype 01' a variation of DI type 1I is debatable , Recent genetic findings have focused attention on the role of the dentin sialo phosphoprotein(DSPP) gene in the etiology of inherited defects of tooth dentin, We have identified novel mlltation( c,727G - > A, p,D243N) at the 243th codon of exon 4 of the DSPP gene in a Korean patient with DI type III The radiographic and histologic features of the patient revealed the classic phenotype of shell teeth These findings sllggest that DI type II and III are not separate diseases bllt rather the phenotypic variation 01' a s ingle disease

A novel indil‘ubin analog‘ 5’ nitro-indirubinoxime(Ol1) inhibits cell proliferation and induces apoptosis again st variolls hllman cancer cell s. ln this stlldy, we performed the microarray analysis to identify genes diffel'enti ally expressed in the KB oral sqllamollS carcinoma cells after treatment with 011 Of the 10‘ 800 genes a nalyzed , 1700 genes(15.7%) showed di fferent expression level in the 011-treated cells with respect to untreated control cel1s Arnong those‘ 263 genes(15, 5%) were down -reg띠 ated and 220 genes(12, 9%) were IIp-regulated more than 2-fold, Functionally related gene clllsters inclllde genes associated with signal transdllction(18, 1%) , especially genes re lated with a poptosis(3, 5%) and cell cycle reglllation(5. 8%) . Our application of microarray ar뻐ysis on 01l-treated 01'외 cancer cells al lows the identifi cati on of candidate genes for providing novel insights into the 011-mediated anti -tllmor actl Vl ty ,