2007 Fiscal Year Final Research Report Summary
Development of molecular target-based therapy of cutaneous squamous cell carcinoma by selective block of PI3K isoforms
| Project/Area Number |
18591231
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Dermatology
|
|---|
| Research Institution | Akita University |
|---|
Principal Investigator |
MANABE Motomu Akita University, School of Medicine, Professor (30138309)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NARITA Tae Akita University, School of Medicine, Assistant Professor (10301061)
TSUDA Masaaki Akita University, School of Medicine, Assistant Professor (30333925)
|
|---|
| Project Period (FY) |
2006 – 2007
|
| Keywords | PI3K / PTEN / SCC / molecular target-based therapy |
|---|
| Research Abstract |
Phosphoinositide 3-kinases (PI3Ks) are a family of lipid kinases that regulate a wide range of cellular processes, among which are cell survival, growth, and proliferation, processes whose misregulation contributes to cancer. There are 4 members in the PI3K class I family, in which the catalytic subunits are p 110α, p 110β, p 110γ, and p 110δ isoforms.
To reveal its role in cancer development, we examined the effect of deleting various isoforms of PI3K (p85α, p 110α, p 110γ, and p 110δ) on epithelial neoplasma in PTEN-/-mice.
Interestingly, we found that either the heterozygous loss of p110α or the homozygous loss of p 110γ led to ecreased incidence of epithelial neoplasma. These results indicate that decreasing the levels of different p 110 subunits can result in decreased PI3K signaling in epidermis, supporting the model that both p110α and p 110γ can function as inhibitors of PI3K signaling in some tissues and thus suppress tumor formation.
Taken together, our results suggest that both the p110α and p 110γ play crucial roles in mediating PI3K signaling in epithelial neoplastic lesions in PTEN-/-mice, and therapeutic approaches that target the PI3K pathway in cancer may exploit such differences between these isoforms.
|
-
-
-
-
[Journal Article] Trichoblastic infundibular cyst2006
Author(s)
Ansai, S., Tsuda, M., Nagato, H., Ni sh imaki, K., Wako, M., Manabe, M., Fukumoto, T., Kimura, T.
-
Journal Title
Am J Dermatopathol 28
Pages: 507-509
Description
「研究成果報告書概要(欧文)」より
-
-
-
-
-
-
