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DNA-PKcs 抑制通过端粒加帽破坏使癌细胞对碳离子照射敏感。

DNA-PKcs inhibition sensitizes cancer cells to carbon-ion irradiation via telomere capping disruption.

机构信息

Department of Heavy Ion Radiation Medicine, Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou, China ; Key Laboratory of Heavy Ion Radiation Biology and Medicine of Chinese Academy of Sciences, Lanzhou, China ; Key Laboratory of Heavy Ion Radiation Medicine of Gansu Province, Lanzhou, China.

出版信息

PLoS One. 2013 Aug 27;8(8):e72641. doi: 10.1371/journal.pone.0072641. eCollection 2013.

Abstract

Heavy-ion irradiation induces a higher frequency of DNA double strand breaks (DSBs) which must be properly repaired. Critical shortening of telomeres can trigger DNA damage responses such as DSBs. Telomeres are very sensitive to oxidative stress such as ionizing radiation. The DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is the central component in the non-homologous end joining (NHEJ) repair complex and participates in telomere maintenance. Therefore, it is expected to enhance the cell killing effect of heavy-ion irradiation via DNA-PKcs inhibition. To test this hypothesis, cellular radiosensitivity was measured by the clonal genetic assay. DNA damage repair was relatively quantified by long PCR. Apoptosis was quantified by flow-cytometric analysis of annexin V/PI double staining, and senescence was analyzed by galactosidase activity. Telomere length was semi-quantified by real-time PCR. P53 and p21 expression was determined by western blotting. Our data demonstrated that MCF-7 and HeLa cells with DNA-PKcs inhibition were more susceptible to carbon-ion irradiation than Those without DNA-PKcs inhibition. Even though NHEJ was inhibited by the DNA-PKcs specific inhibitor, NU7026, most DNA damage induced by carbon-ion irradiation was repaired within 24 hours after irradiation in both cell lines. However, potential lethal damage repair (PLDR) could not restore cellular inactivation in DNA-PKcs inhibited cells. MCF-7 cells showed extensive senescence and accelerated telomere length reduction, while HeLa cells underwent significant apoptosis after irradiation with NU7026 incubation. In addition, both cell lines with shorter telomere were more susceptible to carbon-ion radiation. Our current data suggested that DNA-PKcs inhibition could enhance cellular sensitivity to carbon-ion radiation via disturbing its functional role in telomere end protection. The combination of DNA-PKcs inhibition and carbon-ion irradiation may be an efficient method of heavy-ion therapy.

摘要

重离子辐照诱导更高频率的 DNA 双链断裂 (DSBs),必须正确修复。端粒的严重缩短会引发 DNA 损伤反应,如 DSBs。端粒对电离辐射等氧化应激非常敏感。DNA 依赖性蛋白激酶催化亚基 (DNA-PKcs) 是非同源末端连接 (NHEJ) 修复复合物的核心组成部分,并参与端粒维持。因此,预计通过 DNA-PKcs 抑制来增强重离子辐照的细胞杀伤效应。为了验证这一假设,通过克隆遗传测定来测量细胞放射敏感性。通过长 PCR 相对定量 DNA 损伤修复。通过 Annexin V/PI 双染色的流式细胞术分析来定量细胞凋亡,通过半乳糖苷酶活性分析来分析衰老。通过实时 PCR 半定量端粒长度。通过 Western blot 测定 P53 和 p21 的表达。我们的数据表明,与没有 DNA-PKcs 抑制的细胞相比,抑制 DNA-PKcs 的 MCF-7 和 HeLa 细胞对碳离子辐照更敏感。尽管 NHEJ 被 DNA-PKcs 特异性抑制剂 NU7026 抑制,但在这两种细胞系中,碳离子辐照诱导的大多数 DNA 损伤在辐照后 24 小时内得到修复。然而,潜在致死损伤修复 (PLDR) 不能恢复 DNA-PKcs 抑制细胞中的细胞失活。 MCF-7 细胞表现出广泛的衰老和加速的端粒长度缩短,而 HeLa 细胞在用 NU7026 孵育后经历了显著的凋亡。此外,端粒较短的两种细胞系对碳离子辐射更敏感。我们目前的数据表明,通过干扰 DNA-PKcs 在端粒末端保护中的功能作用,DNA-PKcs 抑制可以增强细胞对碳离子辐射的敏感性。DNA-PKcs 抑制与碳离子辐射的结合可能是重离子治疗的一种有效方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/43aa/3754927/eba2fd866bc1/pone.0072641.g001.jpg

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