STAT3: A Novel Molecular Mediator of Resistance to Chemoradiotherapy

被引:78
作者
Spitzner, Melanie [1 ]
Ebner, Reinhard [2 ]
Wolff, Hendrik A. [3 ]
Ghadimi, B. Michael [1 ]
Wienands, Juergen [4 ]
Grade, Marian [1 ]
机构
[1] Univ Med Gottingen, Dept Gen Visceral & Pediat Surg, Robert Koch Str 40, D-37075 Gottingen, Germany
[2] NCI, Genet Branch, NIH, Bethesda, MD 20892 USA
[3] Univ Med Gottingen, Dept Radiotherapy & Radiooncol, D-37075 Gottingen, Germany
[4] Univ Med Gottingen, Dept Cellular & Mol Immunol, D-37073 Gottingen, Germany
来源
CANCERS | 2014年 / 6卷 / 04期
关键词
STAT3; cancer; radiotherapy; chemoradiotherapy; chemoradiotherapy-resistance; chemoradiotherapy-sensitization; molecular target; SQUAMOUS-CELL CARCINOMA; RADIATION-INDUCED APOPTOSIS; LUNG-CANCER CELLS; ANAPLASTIC THYROID-CARCINOMA; LOCALIZED PROSTATE-CANCER; INVASIVE BLADDER-CANCER; SIGNAL TRANSDUCER; CONSTITUTIVE ACTIVATION; TRANSCRIPTION; ENHANCES RADIOSENSITIVITY;
D O I
10.3390/cancers6041986
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Chemoradiotherapy (CRT) represents a standard treatment for many human cancers, frequently combined with radical surgical resection. However, a considerable percentage of primary cancers are at least partially resistant to CRT, which represents a substantial clinical problem, because it exposes cancer patients to the potential side effects of both irradiation and chemotherapy. It is therefore exceedingly important to determine the molecular characteristics underlying CRT-resistance and to identify novel molecular targets that can be manipulated to re-sensitize resistant tumors to CRT. In this review, we highlight much of the recent evidence suggesting that the signal transducer and activator of transcription 3 (STAT3) plays a prominent role in mediating CRT-resistance, and we outline why inhibition of STAT3 holds great promise for future multimodal treatment concepts in oncology.
引用
收藏
页码:1986 / 2011
页数:26
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