The long noncoding RNA (lncRNA) Eosinophil Granule Ontogeny Transcript (EGOT) has been reported to inhibit the proliferation and migration of glioma cells, and promote the development and progression of gastric cancer through the Hedgehog (Hh) signaling pathway. This study was conducted to assess the role of EGOT in the progression of breast cancer. We observed that EGOT is significantly down‐regulated in breast cancer tissues and cell lines, and EGOT expression is negatively correlated with the Ki67 expression. Overexpression of EGOT in BT549 cells decreased cell viability and migration. In addition, overexpression of EGOT resulted in decreases in expression of key genes in the Hh pathway, including Gli1, smoothened protein, protein patched homolog 1 and Hedgehog‐interacting protein (HHIP). Breast cancer tissues exhibited an increase in Gli1 expressions. Altered expression of Gli1, smoothened protein, protein patched homolog 1 and HHIP caused by EGOT overexpression were fully restored in cells transfected with plasmid complementory DNA (pcDNA) EGOT and treated with purmorphamine, an agonist of the Hh pathway. Cell viability and migration were also restored by purmorphamine. We conclude that lncRNA EGOT may inhibit breast cancer cell viability and migration via inactivation of the Hh pathway.

中文翻译：

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LncRNA EGOT 通过使 Hedgehog 通路失活来降低乳腺癌细胞的活力和迁移。

据报道，长非编码RNA（lncRNA）嗜酸性粒细胞个体发育转录本（EGOT）可抑制胶质瘤细胞的增殖和迁移，并通过Hedgehog（Hh）信号通路促进胃癌的发生和进展。本研究旨在评估EGOT在乳腺癌进展中的作用。我们观察到EGOT在乳腺癌组织和细胞系中显着下调，并且EGOT表达与 Ki67 表达呈负相关。BT549 细胞中EGOT的过度表达会降低细胞活力和迁移。此外，EGOT的过度表达导致Hh通路中关键基因的表达减少，包括Gli1、smoothened Protein、 Protein patchedhomolog 1和Hedgehog-interacting Protein (HHIP)。乳腺癌组织中 Gli1 表达增加。在用质粒互补 DNA (pcDNA) EGOT转染并用 Hh 途径激动剂 purmorphamine 处理的细胞中，由EGOT过表达引起的 Gli1、smoothened 蛋白、蛋白补丁同源物 1 和 HHIP 的表达改变完全恢复。嘌吗啡胺也恢复了细胞活力和迁移。我们得出结论，lncRNA EGOT可能通过 Hh 通路失活来抑制乳腺癌细胞的活力和迁移。