Department of Breast, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, PR China.
Department of Pathology, The Affiliated Cancer Hospital of Zhengzhou University, Zhengzhou, PR China.
Eur J Pharmacol. 2019 Aug 5;856:172407. doi: 10.1016/j.ejphar.2019.172407. Epub 2019 May 25.
The long non-coding RNA (lncRNA) small nucleolar RNA host gene 7 (SNHG7) has been reported to be upregulated and contribute to carcinogenesis, progression and poor prognosis of many cancers. However, expression and function of SNHG7 in breast cancer remain unclear. Herein, we found that SNHG7 was significantly up-regulated in breast cancer tissues and cell lines. SNHG7 knockdown significantly inhibited MCF-7 cell proliferation and invasion, while SNHG7 overexpression dramatically promoted T47D cell proliferation and invasion. Xenograft experiments in vivo showed that SNHG7 knockdown significantly inhibited tumor growth in mice. In terms of mechanism, miR-34a was confirmed to be the target of SNHG7, and SNHG7 could sponge miR-34a to inhibit the expression of miR-34a. In vivo and in vitro experiments both showed that SNHG7 targeted miR-34a and promoted epithelial-to-mesenchymal transition (EMT) initiation and the Notch-1 pathway in breast cancer. In conclusion, SNHG7 promoted breast cancer tumorigenesis and progression by sponging miR-34a through EMT initiation and the Notch-1 pathway. These findings contribute to a better understanding of breast cancer pathogenesis and further provide the theoretical fundamental basis for treatment.
长链非编码 RNA（lncRNA）小核仁 RNA 宿主基因 7（SNHG7）的表达上调被报道与许多癌症的发生、进展和不良预后有关。然而，SNHG7 在乳腺癌中的表达和功能仍不清楚。在此，我们发现 SNHG7 在乳腺癌组织和细胞系中显著上调。SNHG7 敲低显著抑制 MCF-7 细胞的增殖和侵袭，而 SNHG7 过表达则显著促进 T47D 细胞的增殖和侵袭。体内异种移植实验表明，SNHG7 敲低显著抑制了小鼠肿瘤的生长。在机制方面，miR-34a 被证实是 SNHG7 的靶基因，SNHG7 可以通过海绵吸附 miR-34a 来抑制 miR-34a 的表达。体内和体外实验均表明，SNHG7 通过 EMT 起始和 Notch-1 通路靶向 miR-34a 促进乳腺癌的发生和进展。总之，SNHG7 通过 EMT 起始和 Notch-1 通路海绵吸附 miR-34a 促进乳腺癌肿瘤的发生和发展。这些发现有助于更好地理解乳腺癌的发病机制，并为治疗提供了理论基础。
