共 49 条
Targeting polo-like kinase 1, a regulator of p53, in the treatment of adrenocortical carcinoma
被引:25
作者:

Bussey, Kimberly J.
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Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA
Translat Genom Res Inst TGen, Phoenix, AZ 85004 USA Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA

Bapat, Aditi
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Translat Genom Res Inst TGen, Phoenix, AZ 85004 USA Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA

Linnehan, Claire
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Translat Genom Res Inst TGen, Phoenix, AZ 85004 USA Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA

Wandoloski, Melissa
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Translat Genom Res Inst TGen, Phoenix, AZ 85004 USA Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA

Dastrup, Erica
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Translat Genom Res Inst TGen, Phoenix, AZ 85004 USA Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA

Rogers, Erik
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机构:
Translat Genom Res Inst TGen, Phoenix, AZ 85004 USA Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA

Gonzales, Paul
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机构:
Translat Drug Dev, Scottsdale, AZ USA Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA

Demeure, Michael J.
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机构:
Translat Genom Res Inst TGen, Phoenix, AZ 85004 USA Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA
机构:
[1] Arizona State Univ, NantOmics LLC, POB 875001, Tempe, AZ 85287 USA
[2] Translat Genom Res Inst TGen, Phoenix, AZ 85004 USA
[3] Translat Drug Dev, Scottsdale, AZ USA
来源:
CLINICAL AND TRANSLATIONAL MEDICINE
|
2016年
/
5卷
关键词:
Adrenocortical carcinoma;
PLK-1;
p53;
Targeted therapy;
D O I:
10.1186/s40169-015-0080-3
中图分类号:
R73 [肿瘤学];
学科分类号:
100214 ;
摘要:
Background: Adrenocortical carcinoma (ACC) is an aggressive cancer with a 5 year survival rate of 20-30 %. Various factors have been implicated in the pathogenesis of ACC including dysregulation of the G2/M transition and aberrant activity of p53 and MDM2. Polo-like kinase 1 (PLK-1) negatively modulates p53 functioning, promotes MDM2 activity through its phosphorylation, and is involved in the G2/M transition. Gene expression profiling of 44 ACC samples showed that increased expression of PLK-1 in 29 % of ACC. Consequently, we examined PLK-1's role in the modulation of the p53 signaling pathway in adrenocortical cancer. Methods: We used siRNA knock down PLK-1 and pharmacological inhibition of PLK-1 and MDM2 ACC cell lines SW-13 and H295R. We examined viability, protein expression, p53 transactivation, and induction of apoptosis. Results: Knocking down expression of PLK-1 with siRNA or inhibition of PLK-1 by a small molecule inhibitor, BI-2536, resulted in a loss of viability of up to 70 % in the ACC cell lines H295R and SW-13. In xenograft models, BI-2536 demonstrated marked inhibition of growth of SW-13 with less inhibition of H295R. BI-2536 treatment resulted in a decrease in mutant p53 protein in SW-13 cells but had no effect on wild-type p53 protein levels in H295R cells. Additionally, inhibition of PLK-1 restored wild-type p53's transactivation and apoptotic functions in H295R cells, while these functions of mutant p53 were restored only to a smaller extent. Furthermore, inhibition of MDM2 with nutlin-3 reduced the viability of both the ACC cells and also reactivated wild-type p53's apoptotic function. Inhibition of PLK-1 sensitized the ACC cell lines to MDM2 inhibition and this dual inhibition resulted in an additive apoptotic response in H295R cells with wild-type p53. Conclusions: These preclinical studies suggest that targeting p53 through PLK-1 is an attractive chemotherapy strategy warranting further investigation in adrenocortical cancer.
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