The mechanical analysis of nucleic acid-induced cancer selective apoptosis for breast cancer therapy

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K20834
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Obstetrics and gynecology; Tumor therapeutics
• Research Institution: Hokkaido University
• Principal Investigator: Ishikawa Kozo 北海道大学, 遺伝子病制御研究所, 学術研究員 (20624795)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 自然免疫 / 癌細胞選択的アポトーシス / 核酸ナノデリバリー

Outline of Final Research Achievements

Single/double strand RNAs have been reported to induce tumor selective apoptosis in vitro or in vivo experiment and expected as a novel tumor therapy. However, the mechanism that lead to tumor selective apoptosis via IFN (interferon) is controversial, and precise intracellular signaling has not been elucidated.In the present study, an innate sensor RIG-I (retinoic acid-inducible gene-I) is found to evoke tumor selective apoptosis signal without direct involvement of MAVS (mitochondrial antiviral signaling protein) which induce IFN production, by using gene editing tool and proteome analysis in vitro. Moreover, in colorectal cancer metastatic mice model, an artificial nucleic acid 3pRNA is found to induce tumor selective apoptosis without dependent effect of IFN in liver metastatic lesions.
The present results may open a new horizon for the tumor treatment which can avoid the side effect of IFN like fever, depression and general malaise.

Free Research Field

腫瘍免疫