Novel biomarker for tumor anti-angiogenic therapy based on molecular biology

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461938
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General surgery
• Research Institution: Gunma University
• Principal Investigator: Fujii Takaaki 群馬大学, 医学部附属病院, 助教 (40507331)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 腫瘍血管新生 / リンパ節転移 / VEGF / リンパ節外浸潤

Outline of Final Research Achievements

We hypothesized that the mTOR inhibitor-induced anticancer effect is affected by expression of a key angiogenic factor, vascular endothelial growth factor (VEGF). The key observations made in this study can be summarized as follows: 1) administration of rapamycin dose-dependently reduced cell viability of MCF-7, but did not reduce cell viability of HT-29; 2) rapamycin reduced VEGF expression in the culture medium of MCF-7, while rapamycin did not contribute VEGF expression to the culture medium of HT-29; 3) VEGF stimulated cell viability and VEGF inhibition reduced cell viability of MCF-7; and 4) rapamycin dose-dependently restored the cell viability of MCF-7 reduced by rapamycin. These results demonstrate the critical role of VEGF in the action of rapamycin as an anticancer agent on MCF-7. We also revealed that lymph node metastasis and ECI suggest poor prognosis and, especially ECI represent lymphatic aggressive disease and also biological aggressiveness in cases with breast cancer.

Free Research Field

腫瘍外科学