Mechanisms of platinum drug resistance

被引:139
作者
Ohmichi, M
Hayakawa, J
Tasaka, K
Kurachi, H
Murata, Y
机构
[1] Osaka Univ, Sch Med, Dept Obstet & Gynecol, Suita, Osaka 5650871, Japan
[2] Yamagata Univ, Sch Med, Dept Obstet & Gynecol, Yamagata 9909585, Japan
关键词
D O I
10.1016/j.tips.2005.01.002
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Platinum-based drugs are among the most active anticancer agents available and are used widely for the treatment of a variety of human solid tumors. Although patients show high response rates to platinum drugs, most patients develop resistance to these drugs during treatment. Because the acquisition of resistance is a major obstacle to the clinical use of platinum drugs, the processes by which cells develop such resistance are of great interest and efforts have been made to overcome this problem. Both mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K) cascades are involved in resistance to these drugs, and clinical trials of some small-molecule inhibitors of the MAPK and PI3K-Akt cascades to overcome resistance to platinum drugs are ongoing.
引用
收藏
页码:113 / 116
页数:4
相关论文
共 25 条
[1]   The tumor suppressor p16INK4a gene is a regulator of apoptosis induced by ultraviolet light and cisplatin [J].
Al-Mohanna, MA ;
Manogaran, PS ;
Al-Mukhalafi, Z ;
Al-Hussein, KA ;
Aboussekhra, A .
ONCOGENE, 2004, 23 (01) :201-212
[2]   Inhibition of phosphorylation of a forkhead transcription factor sensitizes human ovarian cancer cells to cisplatin [J].
Arimoto-Ishida, E ;
Ohmichi, M ;
Mabuchi, S ;
Takahashi, T ;
Ohshima, C ;
Hayakawa, J ;
Kimura, A ;
Takahashi, K ;
Nishio, Y ;
Sakata, M ;
Kurachi, H ;
Tasaka, K ;
Murata, Y .
ENDOCRINOLOGY, 2004, 145 (04) :2014-2022
[3]   Role of X-linked inhibitor of apoptosis protein in chemoresistance in ovarian cancer: possible involvement of the phosphoinositide-3 kinase/Akt pathway [J].
Cheng, JQ ;
Jiang, XX ;
Fraser, M ;
Li, M ;
Dan, HC ;
Sun, M ;
Tsang, BK .
DRUG RESISTANCE UPDATES, 2002, 5 (3-4) :131-146
[4]   Survival factor-mediated BAD phosphorylation raises the mitochondrial threshold for apoptosis [J].
Datta, SR ;
Ranger, AM ;
Lin, MZ ;
Sturgill, JF ;
Ma, YC ;
Cowan, CW ;
Dikkes, P ;
Korsmeyer, SJ ;
Greenberg, ME .
DEVELOPMENTAL CELL, 2002, 3 (05) :631-643
[5]   Cisplatin resistance and oncogene - a review [J].
Dempke, W ;
Voigt, W ;
Grothey, A ;
Hill, BT ;
Schmoll, HJ .
ANTI-CANCER DRUGS, 2000, 11 (04) :225-236
[6]   PI 3-kinase, Akt and cell survival [J].
Downward, J .
SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY, 2004, 15 (02) :177-182
[7]   PI3K/Akt and apoptosis: size matters [J].
Franke, TF ;
Hornik, CP ;
Segev, L ;
Shostak, GA ;
Sugimoto, C .
ONCOGENE, 2003, 22 (56) :8983-8998
[8]   Biochemical modulation of cisplatin mechanisms of action:: Enhancement of antitumor activity and circumvention of drug resistance [J].
Fuertes, MA ;
Alonso, C ;
Pérez, JM .
CHEMICAL REVIEWS, 2003, 103 (03) :645-662
[9]   Multidrug resistance in cancer: Role of ATP-dependent transporters [J].
Gottesman, MM ;
Fojo, T ;
Bates, SE .
NATURE REVIEWS CANCER, 2002, 2 (01) :48-58
[10]   Inhibition of extracellular signal-regulated protein kinase or c-Jun N-terminal protein kinase cascade, differentially activated by cisplatin, sensitizes human ovarian cancer cell line [J].
Hayakawa, J ;
Ohmichi, M ;
Kurachi, H ;
Ikegami, H ;
Kimura, A ;
Matsuoka, T ;
Jikihara, H ;
Mercola, D ;
Murata, Y .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (44) :31648-31654