Molecular determinants of ovarian cancer chemoresistance: new insights into an old conundrum

被引:78
作者
Ali, Ahmed Y. [1 ,2 ,3 ]
Farrand, Lee [4 ]
Kim, Ji Young [1 ,4 ]
Byun, Sanguine [4 ]
Suh, Jeong-Yong [4 ]
Lee, Hyong Joo [4 ]
Tsang, Benjamin K. [1 ,2 ,3 ,4 ,5 ]
机构
[1] Ottawa Hosp, Res Inst, Chron Dis Program, Ottawa, ON K1Y 4E9, Canada
[2] Univ Ottawa, Dept Cellular Med, Ottawa, ON, Canada
[3] Univ Ottawa, Dept Mol Med, Ottawa, ON, Canada
[4] Seoul Natl Univ, Coll Agr & Life Sci, Dept Agr Biotechnol, Seoul, South Korea
[5] Univ Ottawa, Dept Obstet & Gynecol, Ottawa, ON, Canada
来源
NUTRITION AND PHYSICAL ACTIVITY IN AGING, OBESITY, AND CANCER | 2012年 / 1271卷
基金
加拿大健康研究院; 新加坡国家研究基金会;
关键词
ovarian cancer chemoresistance; p53; PPM1D; PI3K/Akt; functional food compounds; DNA-DAMAGE RESPONSE; ONCOGENIC PHOSPHATASE WIP1; X-LINKED INHIBITOR; PROTEIN-KINASE B; NF-KAPPA-B; CISPLATIN RESISTANCE; AKT PHOSPHORYLATION; TUMOR-SUPPRESSOR; CELL HOMEOSTASIS; OVER-EXPRESSION;
D O I
10.1111/j.1749-6632.2012.06734.x
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Ovarian cancer is the most lethal gynecological malignancy. Cisplatin and its derivatives are first-line chemotherapeutics, and their resistance is a major hurdle in successful ovarian cancer treatment. Understanding the molecular dysregulation underlying chemoresistance is important for enhancing therapeutic outcome. Here, we review two established pathways in cancer chemoresistance. p53 is a major tumor suppressor regulating proliferation and apoptosis, and its mutation is a frequent event in human malignancies. The PI3K/Akt axis is a key oncogenic pathway regulating survival and tumorigenesis by controlling several tumor suppressors, including p53. The interplay between these pathways is well established, although the oncogenic phosphatase PPM1D adds a new layer to this intricate relationship and provides new insights into the processes determining cell fate. Inhibition of the PI3K/Akt pathway by functional food compounds as an adjunct to chemotherapeutics may tip the balance in favor of apoptosis rather than survival, enhancing therapeutic efficacy, and reducing side effects.
引用
收藏
页码:58 / 67
页数:10
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