MiR-320a downregulation is associated with imatinib resistance in gastrointestinal stromal tumors

被引：20

作者：

Gao, Xiaodong ^{[1
]}

Shen, Kuntang ^{[1
]}

Wang, Cuizhong ^{[1
]}

Ling, Jiaqian ^{[1
]}

Wang, Hongshan ^{[1
]}

Fang, Yong ^{[1
]}

Shi, Yuan ^{[2
]}

Hou, Yingyong ^{[2
]}

Qin, Jin ^{[1
]}

Sun, Yihong ^{[1
]}

Qin, Xinyu ^{[1
]}

机构：

[1] Fudan Univ, Zhongshan Hosp, Dept Gen Surg, Shanghai 200032, Peoples R China

[2] Fudan Univ, Zhongshan Hosp, Dept Pathol, Shanghai 200032, Peoples R China

来源：

ACTA BIOCHIMICA ET BIOPHYSICA SINICA | 2014年 / 46卷 / 01期

关键词：

gastrointestinal stromal tumor; imatinib resistant; miR-320a; TYROSINE KINASE; CANCER-CELLS; THERAPY;

D O I：

10.1093/abbs/gmt118

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Gastrointestinal stromal tumor (GIST) is one of the most common mesenchymal tumors of the gastrointestinal tract. Though imatinib improves the outcome, drug resistance remains the major problem for extending patient survival. Genetic mutation of the drug targets is the known mechanism for imatinib resistance. However, it cannot explain all of the phenomena of imatinib resistance, and numerous additional mechanisms have been proposed to account for imatinib resistance in various model systems. In this study, we applied the SYBR-green quantitative polymerase chain reaction-based array approach to screen the differentially expressed miRNAs between primary GIST patients and imatinib-resistant patients. The selected candidate miRNAs were validated in a cohort of 12 GIST patients. We found that low expression of miR-320a was correlated with short time to imatinib resistance, and proposed the potential mechanism of miR-320a for imatinib resistance.

引用

页码：72 / 75

页数：4

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