目的：探讨miR-31-5p/张力蛋白1 基因（tension protein 1，TNS1）分子轴对乳腺癌细胞生物学行为的影响及其放疗抵抗的分子机制。方法：收集2017 年7 月至2017 年12 月南阳市中心医院肿瘤放疗科收治的、经手术切除的21 例乳腺癌患者癌及癌旁组织标本，以及乳腺癌细胞系MCF-7、MDA-MB-231 和SKBR-3，采用qPCR法检测癌组织和癌细胞系中miR-31-5p 的表达水平。通过6 MV-X射线照射MCF-7 细胞，构建放疗抵抗细胞株MCF-7R。随后，采用克隆形成实验、Transwell 小室法和AnnexinV/PI 染色流式细胞术检测过表达/敲降miR-31-5p 对MCF-7 和MCF-7R细胞放疗敏感性的影响；用双荧光素酶报告基因验证miR-31-5p 与TNS1 的靶向关系。结果：乳腺癌组织、细胞系和MCF-7R细胞中miR-31-5p 表达水平显著低于癌旁组织、人正常乳腺上皮细胞MCF-10A和MCF-7 细胞（均P<0.01）。过表达miR-31-5p 显著抑制MCF-7R细胞的侵袭并促进细胞凋亡（均P<0.01），沉默miR-31-5p 在MCF-7 细胞中结果相反。双荧光素酶报告基因法证实TNS1 是miR-31-5p 靶基因。过表达miR-31-5p 通过靶向下调TNS1 显著抑制MCF-7R细胞侵袭能力并促进细胞凋亡（均P<0.01），沉默miR-31-5p 通过上调TNS1 显著促进MCF-7 细胞侵袭和抑制细胞凋亡（均P<0.01），从而上调MCF-7R对放射治疗的敏感性。结论：miR-31-5p/TNS1 分子轴与乳腺癌放疗抵抗存在调控关系，且过表达miR-31-5p 可逆转MCF-7R细胞对放疗抵抗作用。

Objective: To investigate the mechanism of miR-31-5p/tension protein 1 gene (TNS1) axis modulating radiotherapy resistance in breast cancer. Methods: The breast cancer tissues and corresponding para-cancerous tissues of 21 patients with breast cancer,who underwent surgical resection at Department of Cancer Radiotherapy of Nanyang Central Hospital from July 2017 to December 2017, were collected for this study; breast cancer cell lines (MCF-7，MDA-MB-23 and SKBR-3) were also collected; qPCR was applied to detect the expression level of miR-31-5p in breast cancer tissues and cell lines. The radiation resistant cell line MCF-7R was constructed by using 6 MV-X ray radiotherapy treatment. Subsequently, the influence of over-expression/kockdown of miR-31-5p on radiation sensitivity of MCF-7 and MCF-7R cells were detected by colony formation assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. Moreover, luciferase reporter assay was used to verify whether TNS1 was a target gene of miR-31-5p. Results: Compared with para-cancerous tissues, normal mammary epithelial MCF-10A cells and MCF-7 cells, miR-31-5p was low-expressed in breast cancer, cell lines and MCF-7R (all P<0.01). Over-expression of miR-31-5p resulted in inhibited invasion and promoted apoptosis of MCF-7R cells (P<0.01), whereas miR-31-5p knockdown got opposite results in MCF-7 cells. Moreover, luciferase reporter assay confirmed that TNS1 was a target gene of miR-31-5p. Over-expression of miR-31-5p inhibited invasion and increased radio-sensitivity, apoptosis of MCF-7R cell via targeting TNS1 (P<0.01), whereas knockdown of miR-31-5p significantly promoted the invasion but reduced apoptosis of MCF-7R cells (all P<0.01), and further up-regulated the radio-sensitivity of MCF-7R cells.Conclusion: miR-31-5p/TNS1 axis regulates the radiotherapy resistance of breast cancer, and over-expression of miR-31-5p may reverse the resistance of MCF-7R to radiotherapy.