长链非编码 RNA Linc00152 的下调抑制了乳腺癌细胞的活力、侵袭、迁移和上皮间质转化，并逆转了其化疗耐药性。

Down-regulation of lncRNA Linc00152 suppressed cell viability, invasion, migration, and epithelial to mesenchymal transition, and reversed chemo-resistance in breast cancer cells.

机构信息

Department of Breast Surgery, Nanfang Hospital, Southern Medical University, Guangzhou Road, Guangzhou, China.

出版信息

Eur Rev Med Pharmacol Sci. 2018 May;22(10):3074-3084. doi: 10.26355/eurrev_201805_15067.

DOI:10.26355/eurrev_201805_15067

PMID:29863253

Abstract

OBJECTIVE

Breast cancer is one of the most common cancer types in women, and long non-coding RNAs (lncRNAs) were found to play important roles in breast cancer progression. The present study examined the effects of Linc00152 on the breast cancer progression and explored the underlying molecular mechanisms.

MATERIALS AND METHODS

The expression levels of relevant genes in tissues and cells were detected by quantitative Real-time PCR (qRT-PCR) assay. Cell viability, growth, invasion, and migration were measured by CCK-8, colony formation, transwell invasion, and migration assays, respectively. Western blot was used to detect the expression levels of proteins.

RESULTS

The results showed that Linc00152 was highly expressed in the breast cancer tissues compared to their adjacent normal tissues, and Linc00152 was also up-regulated in the breast cancer cell lines compared to normal cell lines. Knock-down of Linc00152 by using siRNAs in breast cancer cell lines (MDA-MB-231 and MCF-7) significantly suppressed cell viability, cell growth, cell invasion and migration as measured by the CCK-8, colony formation, transwell invasion, and migration assays. The qRT-PCR and Western blot results showed that knock-down of Linc00152 suppressed epithelial-mesenchymal transition in breast cancer cell lines. In addition, CCK-8 assay showed that knock-down of Linc00152 in MCF-7/ADR cells reversed the chemo-resistance to doxorubicin.

CONCLUSIONS

Our results suggested the oncogenic role of Linc00152 in the breast cancer progression. Understanding the role of Linc00152 in breast cancer progression may provide a novel therapeutic target for the treatment of breast cancer.

摘要

目的

乳腺癌是女性最常见的癌症类型之一，长链非编码 RNA（lncRNA）被发现在乳腺癌进展中发挥重要作用。本研究探讨了 Linc00152 对乳腺癌进展的影响，并探讨了潜在的分子机制。

材料和方法

采用实时定量 PCR（qRT-PCR）检测组织和细胞中相关基因的表达水平。通过 CCK-8 法、集落形成实验、Transwell 侵袭和迁移实验分别检测细胞活力、生长、侵袭和迁移。Western blot 用于检测蛋白表达水平。

结果

结果表明，与相邻正常组织相比，Linc00152 在乳腺癌组织中高表达，与正常细胞系相比，Linc00152 在乳腺癌细胞系中也上调。在乳腺癌细胞系（MDA-MB-231 和 MCF-7）中使用 siRNA 敲低 Linc00152 显著抑制细胞活力、细胞生长、细胞侵袭和迁移，通过 CCK-8、集落形成、Transwell 侵袭和迁移实验测量。qRT-PCR 和 Western blot 结果表明，敲低 Linc00152 抑制了乳腺癌细胞系中的上皮-间充质转化。此外，CCK-8 实验表明，敲低 MCF-7/ADR 细胞中的 Linc00152 逆转了对阿霉素的耐药性。