MicroRNA-302 replacement therapy sensitizes breast cancer cells to ionizing radiation.
MicroRNA-302 replacement therapy sensitizes breast cancer cells to ionizing radiation.
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DOI：
10.1007/s11095-012-0936-9
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发表时间：
2013-04
影响因子：
3.7
通讯作者：
Shim, Hyunsuk
中科院分区：
文献类型：
--
作者：
Liang, Zhongxing;Ahn, Jeffrey;Guo, Donna;Votaw, John R.;Shim, Hyunsuk
实体瘤可能对放射治疗产生耐药性或产生耐药性。本研究的目的是探讨microRNA-302是否参与了放射耐药，是否可以作为增敏剂来提高乳腺癌细胞对放射治疗的敏感性。分析MiR-302在耐辐射细胞系中的表达水平，并与亲本细胞系进行比较。此外，我们在体外和体内研究了miR-302的强制表达是否使放射耐药乳腺癌细胞对电离辐射敏感。MiR-302在辐照的乳腺癌细胞中下调。此外，miR-302a的表达水平与AKT1和RAD52的表达水平呈负相关，而AKT1和RAD52是辐射抗性的两个关键调节因子。更有希望的是，miR-302a在体外和体内使放射耐药乳腺癌细胞对放射治疗增敏，并降低AKT1和RAD52的表达。我们的研究结果表明，miR-302表达的降低赋予了放射抗性，miR-302基线表达的恢复使乳腺癌细胞对放疗敏感。这些数据表明miR-302是一种潜在的放疗增敏剂。
Solid tumors can be resistant or develop resistance to radiotherapy. The purpose of this study is to explore whether microRNA-302 is involved in radioresistance and can be exploited as a sensitizer to enhance sensitivity of breast cancer cells to radiation therapy. MiR-302 expression levels in radioresistant cell lines were analyzed in comparison with their parent cell lines. Furthermore, we investigated whether enforced expression of miR-302 sensitized radioresistant breast cancer cells to ionizing radiation in vitro and in vivo. MiR-302 was downregulated in irradiated breast cancer cells. Additionally, the expression levels of miR-302a were inversely correlated with those of AKT1 and RAD52, two critical regulators of radioresistance. More promisingly, miR-302a sensitized radioresistant breast cancer cells to radiation therapy in vitro and in vivo and reduced the expression of AKT1 and RAD52. Our findings demonstrated that decreased expression of miR-302 confers radioresistance and restoration of miR-302 baseline expression sensitizes breast cancer cells to radiotherapy. These data suggest that miR-302 is a potential sensitizer to radiotherapy.
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