LINP1 facilitates DNA damage repair through non-homologous end joining (NHEJ) pathway and subsequently decreases the sensitivity of cervical cancer cells to ionizing radiation.
LINP1 facilitates DNA damage repair through non-homologous end joining (NHEJ) pathway and subsequently decreases the sensitivity of cervical cancer cells to ionizing radiation.
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LINP1通过非同源末端连接（NHEJ）途径促进DNA损伤修复，从而降低宫颈癌细胞对电离辐射的敏感性。
DOI：
10.1080/15384101.2018.1442625
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发表时间：
2018
期刊：
影响因子：
--
通讯作者：
Sun X
中科院分区：
文献类型：
--
作者：
Wang X;Liu H;Shi L;Yu X;Gu Y;Sun X
非同源末端连接（NHEJ）途径1（LINP 1）中的LncRNA是促进三阴性乳腺癌（TNBC）中的治疗抗性的lncRNA。然而，LINP 1在宫颈癌中的表达和功能尚未完全了解。在这项研究中，我们评估了LINP 1在宫颈癌组织和细胞系中的表达水平。我们发现LINP 1与NHEJ蛋白（Ku 80和DNA-PKcs）相关。LINP 1从细胞质易位到细胞核响应辐射。此外，LINP 1敲低显著增加切割的半胱天冬酶3和PARP的水平，导致电离辐射（IR）后细胞凋亡增强。LINP 1基因敲低的细胞表现出延迟修复的DNA双链断裂（DSB）后IR。最后，LINP 1基因敲低增加Hela S3细胞的放射敏感性。这些结果表明LINP 1通过NHEJ途径促进DSB修复，因此可能作为宫颈癌的预后标志物和治疗的潜在靶点。
LncRNA in non-homologous end joining (NHEJ) pathway 1 (LINP1) is an lncRNA which promotes therapeutic resistance in triple-negative breast cancer (TNBC). However, the expression and function of LINP1 in cervical cancer is not yet well-understood. In this study, we evaluated the expression levels of LINP1 in tumor tissues and cell lines of cervical cancer. We found that LINP1 associates with NHEJ proteins (Ku80 and DNA-PKcs). LINP1 translocates from cytosol to nucleus in response to irradiation. In addition, LINP1 knockdown significantly increases the levels of cleaved caspase3 and PARP, leading to enhanced cell apoptosis after ionizing radiation (IR). LINP1-knockdown cells showed delayed repairs of DNA double-strand breaks (DSBs) after IR. Finally, LINP1 knockdown increases radiosensitivity of Hela S3 cells. These results suggest that LINP1 facilitates DSBs repair through NHEJ pathway and may thus serve as a prognostic marker and a potential target for the therapy of cervical cancer.
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