Abstract：
Breast cancer is a global disease and a cause of cancer-related deaths in women. Long non-coding RNAs (lncRNAs) perform important functions in biological processes. The aim of this study was to verify the functions and regulatory mechanisms of linc01152 in breast cancer. Relative expression of linc01152 was measured using RT-PCR. siRNAs targeting linc01152 were designed to inhibit its expression. Cell viability, cell invasion, and migration capacities were determined using CCK-8 and Transwell assays. Downstream targets, miRNAs, and mRNAs were predicted and validated using luciferase reporter assay. The expression of linc01152 in breast cancer cells was higher than that in normal breast cells, with BT474 and MDA-MB-468 cell lines presenting the highest expression levels of linc01152. The inhibition of linc01152 expression led to lower cell viability and attenuated cell migration and invasion. The regulatory network of linc01152-miR-320a-MTDH was validated using luciferase reporter assay. The inhibition of miR-320a expression reversed the effect of si-linc01152 on cell viability, migration, and invasion. Taken together, the linc01152-miR-320a-MTDH regulatory network is correlated with the pathogenesis of breast cancer.
摘要：
乳腺癌是一种全球性疾病，也是女性癌症相关死亡的原因。长链非编码RNA（lncRNA）在生物过程中发挥重要作用。本研究旨在验证linc01152在乳腺癌中的功能和调控机制。使用RT-PCR测量linc01152的相对表达。靶向linc01152的siRNA被设计为抑制其表达。细胞活力，细胞入侵，使用CCK-8和Transwell测定法确定迁移能力。下游目标,miRNA,和mRNA的预测和验证使用荧光素酶报告分析。linc01152在乳腺癌细胞中的表达高于正常乳腺细胞，BT474和MDA-MB-468细胞系呈现最高表达水平的linc01152。抑制linc01152表达导致较低的细胞活力和减弱的细胞迁移和侵袭。使用荧光素酶报告基因测定验证linc01152-miR-320a-MTDH的调控网络。miR-320a表达的抑制逆转了si-linc01152对细胞活力的影响，迁移,和入侵。一起来看,linc01152-miR-320a-MTDH调控网络与乳腺癌的发病机制相关。
