| Project/Area Number |
25860282
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Human pathology
|
|---|
| Research Institution | Nihon University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
|---|
| Keywords | 乳癌 / アポクリン癌 / オートファジー / 脂質代謝 / p62 / PGC1alpha |
|---|
| Outline of Final Research Achievements |
In the recent years, metabolism-related factors have been elucidated as a cause in the increase of the cancer cells and cancerization of normal cells. In this study, three new findings have been established through investigations of lipid metabolic and autophagic status in apocrine carcinoma, which is categorized as a special type of breast carcinoma, and whether or not they relate to cell proliferation. Firstly, stimulation of lipid metabolism and impairment of autophagy are speculated in apocrine carcinomas by contrasting PGC1α and p62 expression within apocrine and non-apocrine carcinomas. Secondly, immunohistochemical analysis of p62 is useful for differential diagnosis of apocrine carcinoma and apocrine metaplasia of the breast. Finally, knockdown of p62 resulted in a reduction of cell proliferative activity in breast cancer cell lines of the apocrine type, indicating that p62 could be a therapeutic target in apocrine carcinoma.
|
