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小核仁 RNA SNORA71A 通过维持乳腺癌中 ROCK2 mRNA 的稳定性促进上皮-间充质转化。

Small nucleolar RNA SNORA71A promotes epithelial-mesenchymal transition by maintaining ROCK2 mRNA stability in breast cancer.

机构信息

Cancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Department of Thyroid and Breast Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Mol Oncol. 2022 May;16(9):1947-1965. doi: 10.1002/1878-0261.13186. Epub 2022 Mar 30.

DOI:10.1002/1878-0261.13186
PMID:35100495
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9067147/
Abstract

Metastasis is the primary reason of death in patients with cancer. Small nucleolar noncoding RNAs (snoRNAs) are conserved 60-300 nucleotide noncoding RNAs, involved in post-transcriptional regulation of mRNAs and noncoding RNAs. Despite their essential roles in cancer, the roles of snoRNAs in epithelial-mesenchymal transition (EMT)-induced metastasis have not been studied extensively. Here, we used small RNA sequencing to screen for snoRNAs related to EMT and breast cancer metastasis. We found a higher expression of SNORA71A in metastatic breast cancer tissues compared to nonmetastatic samples. Additionally, SNORA71A promoted the proliferation, migration, invasion and EMT of MCF-7 and MDA-MB-231 cells. Mechanistically, SNORA71A elevated mRNA and protein levels of ROCK2, a negative regulator of TGF-β signaling. Rescue assays showed ROCK2 abrogated the SNORA71A-mediated increase in proliferation, migration, invasion and EMT. Binding of SNORA71A to mRNA stability regulatory protein G3BP1, increased ROCK2 mRNA half-life. Furthermore, G3BP1 depletion abolished the SNORA71A-mediated upregulation of ROCK2. In vivo, SNORA71A overexpression promoted breast tumor growth, and SNORA71A knockdown inhibited breast cancer growth and metastasis. We suggest SNORA71A enhances metastasis of breast cancer by binding to G3BP1 and stabilizing ROCK2.

摘要

转移是癌症患者死亡的主要原因。小核仁非编码 RNA（snoRNA）是保守的 60-300 个核苷酸的非编码 RNA，参与 mRNA 和非编码 RNA 的转录后调控。尽管 snoRNA 在癌症中具有重要作用，但它们在上皮-间充质转化（EMT）诱导的转移中的作用尚未得到广泛研究。在这里，我们使用小 RNA 测序筛选与 EMT 和乳腺癌转移相关的 snoRNA。我们发现转移性乳腺癌组织中 SNORA71A 的表达高于非转移性样本。此外，SNORA71A 促进 MCF-7 和 MDA-MB-231 细胞的增殖、迁移、侵袭和 EMT。在机制上，SNORA71A 上调了 ROCK2 的 mRNA 和蛋白水平，ROCK2 是 TGF-β 信号的负调节剂。挽救实验表明，ROCK2 逆转了 SNORA71A 介导的增殖、迁移、侵袭和 EMT 的增加。SNORA71A 与 mRNA 稳定性调节蛋白 G3BP1 结合，增加了 ROCK2 mRNA 的半衰期。此外，G3BP1 的耗竭消除了 SNORA71A 对 ROCK2 的上调作用。在体内，SNORA71A 的过表达促进了乳腺癌肿瘤的生长，而 SNORA71A 的敲低抑制了乳腺癌的生长和转移。我们认为 SNORA71A 通过与 G3BP1 结合并稳定 ROCK2 来增强乳腺癌的转移。

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