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2016 Fiscal Year Final Research Report

Reverse Glycomics Clarification of Resistance Mechanism for Leukemia Cell and Development of Diagnosis Method for Antitumor Drug Resistance

Research Project

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Project/Area Number 26505008
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field オミクス計測科学
Research InstitutionHiroshima University

Principal Investigator

Nakano Miyako  広島大学, 先端物質科学研究科, 准教授 (40397724)

Project Period (FY) 2014-04-01 – 2017-03-31
Keywords糖鎖分析 / 白血病 / 薬剤耐性 / グライコミクス / 診断法
Outline of Final Research Achievements

The main treatment of leukemia is chemotherapy using antitumor drugs, but the acquisition of drug resistance often makes treatment continuation impossible. The mechanism of acquired drug resistance must be elucidated. We focused on glycan structures on cell-membrane proteins. A leukemia cell line (CEM) was selected for acquired drug resistance against an antitumor drug (dEpoB), and glycan structures on the cell-membrane proteins was analyzed. The resistant cell line (CEM/dEpoB) showed a significant decrease of 2-6 sialylated N-glycans. The reduction was cause of 2-6 sialyltransferase 1 (ST6GAL1) gene. To ascertain the cause-and-effect relationship between reduction of 2-6 sialylated N-glycans and acquired drug resistance, we knock-downed and transfected the ST6GAL1 gene. The CEM with the knock-down ST6GAL1 gene showed acquired drug resistance. This result suggests that reduction in the 2-6 sialylation could be the cause of dEpoB-resistance acquisition.

Free Research Field

糖鎖分析

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Published: 2018-03-22  

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