miR-1307-3p通过靶向ISM1促进乳腺癌细胞的增殖和迁移

目的 探讨miR-1307-3p通过靶向ISM1促进乳腺癌细胞增殖和迁移的分子机制。方法 （1）利用TCGA数据库分析miR-1307-3p在乳腺癌患者中的表达水平及其与临床指标的关系。（2）利用qPCR、CCK-8实验、细胞划痕实验和流式细胞术检测过表达或沉默miR-1307-3p后乳腺癌MCF-7细胞miR-1307-3p表达、细胞增殖、迁移和凋亡水平变化。（3）生物信息学分析软件预测 miR-1307-3p 的靶基因，同时采用双荧光素酶实验进行验证。结果miR-1307-3p在乳腺癌细胞及乳腺癌组织中均显著上调。miR-1307-3p过表达可促进MCF-7细胞增殖和迁移；而miR-1307-3p inhibitor则抑制细胞迁移，并诱导凋亡。ISM1可能是miR-1307-3p的靶基因。乳腺癌组织中ISM1表达水平明显低于正常乳腺组织，且与临床病理分期有关。 结论miR-1307-3p可促进乳腺癌细胞增殖和迁移，可能通过调控ISM1基因而影响乳腺癌的发生发展。

MiR-1307-3p promotes the proliferation and migration of breast cancer cells by targeting ISM1 #br#

Objective To explore the possible molecular mechanism of miR-1307-3p in promoting proliferation andmigration by targeting ISM1 in breast cancer cells. Methods (1) Cancer Genome Atlas (TCGA) database was used toanalyze the expression level of miR-1307-3p and its relationship with clinical indicators in breast cancer patients. (2)qPCR, CCK-8 assay, Scratch test and flow cytometry were used to detect the effects of miR-1307-3p over-expression orsilence on the expression of miR-1307-3p, cell proliferation, migration and apoptosis in breast cancer MCF-7 cells,respectively. (3) The target gene of mir-1307-3p was predicted by bioinformatics analysis, and verified by double luciferasereporter gene experiment. Results The relative expression levels of miR-1307-3p were significantly up-regulated both inbreast cancer cell lines and breast cancer tissues. Overexpression of miR-1307-3p significantly promoted cell proliferationand migration in MCF-7 cells; on the contrary, miR-1307-3p inhibitor significantly inhibited cell migration and inducedcell apoptosis. ISM1 may be the target genes of miR-1307-3p. The expression level of ISM1 was significantly lower in breastcancer tissues than that in normal breast tissues, and was significantly correlated with clinical stages. Conclusion MiR-1307-3p can promote the proliferation and migration of breast cancer cells, which may affect the occurrence anddevelopment of breast cancer by targeting ISM1 gene.