2005 Fiscal Year Final Research Report Summary
A study of cell survival mechanisms for apoptosis-resistant oral squamous cell carcinoma cell line
| Project/Area Number |
15592137
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Surgical dentistry
|
|---|
| Research Institution | TOKYO DENTAL COLLEGE (2004-2005)
Toho University (2003) |
|---|
Principal Investigator |
SAKAI Takayuki TOKYO DENTAL COLLEGE, DEPARTMENT OF DENTISTRY, LECTURER, 歯学部, 講師 (60260577)
|
|---|
| Project Period (FY) |
2003 – 2005
|
| Keywords | Head and Neck Cancer / Apoptosis / Cell Survival / Phospholipase D / Gene Supression / siRNA |
|---|
| Research Abstract |
Lactoferrin (Lfn) show multi biological function including host defense against not only bacteria and virus but also malignant neoplasm. We previously reported that Lfn peptides (Lfn-p), produced by acid-pepsin hydrolysis of Lfn, induced apaptosis through JNK activation in human oral squamous cell carcinoma cell lines, SAS. (Sakai T et al., J Pharmacol Sci 98,2005) In contrast, we found that Lf-p-induced phospholipase D (PLD) activation in other squamous cell carcinoma cell line, HSC-4, survived in Lf-p-treatment. In the present study, we examined the effect of knockdown of endogenous PLD by small interference RNA (siRNA) on survival signaling activated with Lfn-p in HSC-4 cells. Both PLD1 and 2 were expressed in the cells. The reduction of expression level of PLD1, not PLD2, by siRNA transfection suppressed Lfn-p-induced PLD activity. Lfn-p-induced Akt phosphorylation, well-known survival signaling were also suppressed with PLD activity. Furthermore, JNK phosphorylaiton accompanied by Lfn-p-induced apoptosis in HSC-4 cells was increased in PLD1 knockdown cells. These results suggested that PLD1 was involved in cell survival through PI3K/Akt /JNK pathway in HSC-4 cells.
|
Research Products
(8 results)
