ENO1 的沉默抑制了人乳腺癌细胞的增殖、迁移和侵袭。

Silencing of ENO1 inhibits the proliferation, migration and invasion of human breast cancer cells.

机构信息

Morphology Teaching and Research section, XiZang Minzu University Health Science Center, Xianyang, Shaanxi, China, 712082.

出版信息

J BUON. 2020 Mar-Apr;25(2):696-701.

PMID:32521855

Abstract

PURPOSE

Studies have shown that α-enolase ENO1 is involved in the regulation of cancer cell proliferation and metastasis. However, the role of ENO1 is yet to be explored in breast cancer. This study was undertaken to explore the role and therapeutic potential of ENO1 in breast cancer.

METHODS

Expression analysis was carried out by qRT-PCR. Transfections were performed by Lipofectamine 2000 reagent. WST-1 assay was used for cell viability. Wound healing assay was used for cell migration analysis. Western blot analysis was used to determine protein expression.

RESULTS

The results showed that the expression of ENO1 was significantly upregulated in breast cancer by up to 4-fold. Silencing of ENO1 caused significant decline in the proliferation rate and colony formation of the SK-BR-3 breast cancer cells. The decrease in the proliferation rate of the ENO1 cells was due to the induction of apoptosis as revealed by DAPI staining. Annexin V/propidium iodide (PI) showed a significant increase in the apoptotic SK-BR-3 cells. The apoptosis percentage was 2.17 in si-NC and 23.1% in si-ENO1 transfected SK-BR-3 cells. The apoptosis induction was also accompanied by increase in Bax and decrease in Bcl-2 expression. ENO1 silencing also resulted in the arrest of the SK-BR-3 cells in the G2/M phase of the cell cycle which was also associated with depletion of Cdc2, Cdc25 and cyclin B1 expression levels. ENO1 silencing also caused decrease in the migration and invasion of the SK-BR-3 cells as revealed by the wound healing and transwell assays.

CONCLUSION

These findings suggest that ENO1 has oncogenic properties in breast cancer which can be exploited in breast cancer treatment.

摘要

目的

研究表明，α-烯醇酶 ENO1 参与了癌细胞增殖和转移的调控。然而，ENO1 在乳腺癌中的作用尚未被探索。本研究旨在探讨 ENO1 在乳腺癌中的作用和治疗潜力。

方法

通过 qRT-PCR 进行表达分析。通过 Lipofectamine 2000 试剂进行转染。WST-1 测定法用于细胞活力测定。划痕愈合试验用于细胞迁移分析。Western blot 分析用于测定蛋白表达。

结果

结果表明，ENO1 在乳腺癌中的表达显著上调了 4 倍。ENO1 的沉默导致 SK-BR-3 乳腺癌细胞的增殖率和集落形成显著下降。ENO1 细胞增殖率的下降是由于诱导凋亡，DAPI 染色证实了这一点。Annexin V/碘化丙啶（PI）显示 SK-BR-3 细胞中凋亡明显增加。si-NC 中的凋亡百分比为 2.17%，而在 si-ENO1 转染的 SK-BR-3 细胞中为 23.1%。凋亡诱导也伴随着 Bax 的增加和 Bcl-2 表达的减少。ENO1 沉默还导致 SK-BR-3 细胞在细胞周期的 G2/M 期停滞，这也与 Cdc2、Cdc25 和细胞周期蛋白 B1 表达水平的耗竭有关。ENO1 沉默还导致 SK-BR-3 细胞的迁移和侵袭减少，划痕愈合和 Transwell 试验证实了这一点。