Role of PTPRZ1 to maintain cancer stemness in small-cell lung carcinoma
Project/Area Number |
24700990
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Tumor biology
|
Research Institution | National Center of Neurology and Psychiatry |
Principal Investigator |
MAKINOSHIMA Hideki 独立行政法人国立がん研究センター, 臨床開発センター, 研究員 (30510573)
|
Project Period (FY) |
2012-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | がん幹細胞 / チロシンフォスファターゼ / 肺小細胞がん / PTPRZ1 / フォスファターゼ / チロシンリン酸化 / 分子標的療法 / 幹細胞 |
Research Abstract |
Because small-cell lung carcinoma (SCLC) is still a disease with a poor prognosis and limited treatment options, there is an urgent need to develop targeted molecular agents for this diseases. We screened cell lines and paraffin-embedded tissues from a variety of pathological phenotypes to examine PTPRZ1 expression. Here we show that PTPRZ1 is highly expressed in SCLC cell lines and exists in human SCLC tissues. In addition, we found that PTPRZ1 actually has an important oncogenic role in tumor progression in the murine xenograft model. These results imply that PTPRZ1 could be a feasible cell-surface marker to isolate cancer stem cells of SCLC.To test this idea, we established to separate PTPRZ1 positive cells (PTPRZ1+) from PTPRZ1 negative cells (PTPRZ1-) using anti-PTPRZ1 antibody. However, isolated SCLC cells were technically impossible to maintain cell culture in vitro. Therefore, we could not characterize whether PTPRZ1+ cells might have a feature of cancer stem cells.
|
Report
(3 results)
Research Products
(4 results)