Background

The lacking of estrogen, progesterone and ERBB2 receptor makes the therapy of Triple negative breast cancer (TNBC) is particularly challenging. Accumulating evidences has demonstrated the dysfunction and critical roles of microRNAs (miRNAs) in TNBC.

Objective

Explore the role of miR-506-3p in TNBC and evaluate the clinical significance of miR-506-3p.

Results

miR-506-3p expression was significantly decreased in TNBC and correlated with the worst status of TNBC patients. miR-506-3p overexpression repressed the proliferation, migration and induced cell cycle arrest as well as apoptosis of TNBC cells. Mechanistically, SNAI2 was identified as a target of miR-506-3p in TNBC cells. Consistently, SNAI2 was overexpressed in TNBC and inversely correlated with miR-506-3p level. Transfection of SNAI2 abolished the inhibitory role of miR-506-3p in regulating the malignant phenotypes of TNBC cells.

Conclusions

These results demonstrated the suppressive function of miR-506-3p in TNBC via targeting SNAI2, indicating the possible application of miR-506-3p in TNBC treatment.

中文翻译：

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microRNA-506-3p 通过靶向 SNAI2 抑制三阴性乳腺癌细胞的增殖

背景

由于缺乏雌激素、孕激素和 ERBB2 受体，三阴性乳腺癌 (TNBC) 的治疗尤其具有挑战性。越来越多的证据已经证明了微小 RNA (miRNA) 在 TNBC 中的功能障碍和关键作用。

客观的

探讨 miR-506-3p 在 TNBC 中的作用并评价 miR-506-3p 的临床意义。

结果

miR-506-3p 表达在 TNBC 中显着降低，并且与 TNBC 患者的最差状态相关。miR-506-3p 过表达抑制了 TNBC 细胞的增殖、迁移和诱导的细胞周期停滞以及凋亡。从机制上讲，SNAI2 被确定为 TNBC 细胞中 miR-506-3p 的靶标。一致地，SNAI2 在 TNBC 中过度表达并且与 miR-506-3p 水平呈负相关。SNAI2的转染消除了miR-506-3p在调节TNBC细胞恶性表型中的抑制作用。

结论

这些结果证明了 miR-506-3p 通过靶向 SNAI2 在 TNBC 中的抑制功能，表明 miR-506-3p 在 TNBC 治疗中的可能应用。