HMGA-targeted phosphorothioate DNA aptamers increase sensitivity to gemcitabine chemotherapy in human pancreatic cancer cell lines

被引：20

作者：

Watanabe, Miki ^{[1
]}

Sheriff, Sulaiman ^{[2
]}

Lewis, Kenneth B. ^{[1
]}

Tinch, Stuart L. ^{[1
]}

Cho, Junho ^{[1
]}

Balasubramaniam, Ambikaipakan ^{[2
,3
,4
]}

Kennedy, Michael A. ^{[1
]}

机构：

[1] Miami Univ, Dept Chem & Biochem, Oxford, OH 45056 USA

[2] Univ Cincinnati, Med Ctr, Dept Surg, Cincinnati, OH 45267 USA

[3] Shriners Hosp Children, Cincinnati, OH 45229 USA

[4] Cincinnati Vet Affairs Med Ctr, Cincinnati, OH 45220 USA

来源：

CANCER LETTERS | 2012年 / 315卷 / 01期

基金：

美国国家卫生研究院;

关键词：

HMGA; DNA aptamer; Pancreatic cancer; Gemcitabine; AsPC-1; EXPRESS HIGH-LEVELS; RIBONUCLEOTIDE REDUCTASE; CHROMOSOMAL-PROTEINS; BINDING DOMAIN; CROSS-LINKING; ANTITUMOR; THERAPY; GROWTH; GENE; INHIBITION;

D O I：

10.1016/j.canlet.2011.10.005

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Elevated high mobility group A (HMGA) protein expression in pancreatic cancer cells is correlated with resistance to the chemotherapy agent gemcitabine. Here, we demonstrate use of HMGA-targeted AT-rich phosphorothioate DNA (AT-sDNA) aptamers to suppress HMGA carcinogenic activity. Cell growth of human pancreatic cancer cells (AsPC-1 and Miapaca-2) transfected with AT-sDNA were monitored after treatment with gemcitabine. Significant increases in cell death in AT-sDNA transfected cells compared to non-AT-rich sDNA treated cells were observed in both cell lines. The data indicate the potential use of HMGA targeted DNA aptamers to enhance chemotherapy efficacy in pancreatic cancer treatment. (C) 2011 Elsevier Ireland Ltd. All rights reserved.

引用

页码：18 / 27

页数：10

共 40 条

[1]

Abe N, 2000, CANCER RES, V60, P3117

[2] An increased high-mobility group A2 expression level is associated with malignant phenotype in pancreatic exocrine tissue [J].

Abe, N ;

Watanabe, T ;

Suzuki, Y ;

Matsumoto, N ;

Masaki, T ;

Mori, T ;

Sugiyama, M ;

Chiappetta, G ;

Fusco, A ;

Atomi, Y .

BRITISH JOURNAL OF CANCER, 2003, 89 (11) :2104-2109

[3]

[Anonymous], J HERED

[4] FR900482 class of anti-tumor drugs cross-links oncoprotein HMG I/Y to DNA in vivo [J].

Beckerbauer, L ;

Tepe, JJ ;

Cullison, J ;

Reeves, R ;

Williams, RM .

CHEMISTRY & BIOLOGY, 2000, 7 (10) :805-812

[5] INHIBITION OF RIBONUCLEOTIDE REDUCTASE BY 2'-SUBSTITUTED DEOXYCYTIDINE ANALOGS - POSSIBLE APPLICATION IN AIDS TREATMENT [J].

BIANCHI, V ;

BORELLA, S ;

CALDERAZZO, F ;

FERRARO, P ;

BIANCHI, LC ;

REICHARD, P .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (18) :8403-8407

[6]

Bustin M, 1996, PROG NUCLEIC ACID RE, V54, P35, DOI 10.1016/S0079-6603(08)60360-8

[7]

Chiappetta G, 1996, ONCOGENE, V13, P2439

[8] Biochemical and physicochemical properties of phosphorodithioate DNA [J].

Cummins, L ;

Graff, D ;

Beaton, G ;

Marshall, WS ;

Caruthers, MH .

BIOCHEMISTRY, 1996, 35 (26) :8734-8741

[9] PURIFICATION AND POSTSYNTHETIC MODIFICATIONS OF FRIEND-ERYTHROLEUKEMIC CELL HIGH MOBILITY GROUP PROTEIN HMG-I [J].

ELTON, TS ;

REEVES, R .

ANALYTICAL BIOCHEMISTRY, 1986, 157 (01) :53-62

[10]

Fedele M, 1996, CANCER RES, V56, P1896

← 1 2 3 4 →