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SNORA72激活Notch1/c-Myc信号通路以促进卵巢癌细胞的干性转化。

SNORA72 Activates the Notch1/c-Myc Pathway to Promote Stemness Transformation of Ovarian Cancer Cells.

作者信息

Zhang Liwen, Ma Rong, Gao Mengcong, Zhao Yanyun, Lv Xuemei, Zhu Wenjing, Han Li, Su Panpan, Fan Yue, Yan Yuanyuan, Zhao Lin, Ma Heyao, Wei Minjie, He Miao

机构信息

Department of Pharmacology, School of Pharmacy, China Medical University, Shenyang, China.

Liaoning Key Laboratory of Molecular Targeted Anti-Tumor Drug Development and Evaluation, China Medical University, Shenyang, China.

出版信息

Front Cell Dev Biol. 2020 Nov 3;8:583087. doi: 10.3389/fcell.2020.583087. eCollection 2020.

DOI:10.3389/fcell.2020.583087
PMID:33224949
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7669759/
Abstract

Cancer stem cells (CSCs) are responsible for the migration and recurrence of cancer progression. Small nucleolar RNAs (snoRNAs) play important roles in tumor development. However, how snoRNAs contribute to the regulation of the stemness of ovarian CSCs (OCSCs) remains unclear. In the present study, we found that SNORA72 was significantly upregulated in OVCAR-3 spheroids (OS) and CAOV-3 spheroids (CS) with the OCSC characteristics attained by serum-free culture in a suspension of OVCAR-3 (OV) and CAOV-3 (CA) cells. The overexpression of SNORA72 increased self-renewal abilities and migration abilities in OV and CA cells and upregulated the expressions of the stemness markers Nanog, Oct4, and CD133. In addition, the ectopic expression of SNORA72 can elevate the messenger RNA (mRNA) and protein expression levels of Notch1 and c-Myc in parental cells. The opposite results were observed in SNORA72-silenced OCSCs. Moreover, we found that Notch1 knockdown inversed the migration abilities and self-renewal abilities raised by overexpressing SNORA72. In summary, stemness transformation of ovarian cancer cells can be activated by SNORA72 through the Notch1/c-Myc pathway. This study introduces a novel therapeutic strategy for improving the treatment efficiency of ovarian cancer.

摘要

癌症干细胞（CSCs）是癌症进展过程中迁移和复发的原因。小核仁RNA（snoRNAs）在肿瘤发展中发挥重要作用。然而，snoRNAs如何促进卵巢癌干细胞（OCSCs）干性的调控仍不清楚。在本研究中，我们发现，在通过将OVCAR-3（OV）和CAOV-3（CA）细胞悬浮培养于无血清条件下获得具有OCSC特征的OVCAR-3球状体（OS）和CAOV-3球状体（CS）中，SNORA72显著上调。SNORA72的过表达增加了OV和CA细胞的自我更新能力和迁移能力，并上调了干性标志物Nanog、Oct4和CD133的表达。此外，SNORA72的异位表达可提高亲本细胞中Notch1和c-Myc的信使核糖核酸（mRNA）和蛋白质表达水平。在SNORA72沉默的OCSCs中观察到相反的结果。此外，我们发现Notch1敲低可逆转因过表达SNORA72而提高的迁移能力和自我更新能力。总之，SNORA72可通过Notch1/c-Myc途径激活卵巢癌细胞的干性转化。本研究引入了一种提高卵巢癌治疗效率的新治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be62/7669759/ba409ea3f914/fcell-08-583087-g007.jpg
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SNORD89 promotes stemness phenotype of ovarian cancer cells by regulating Notch1-c-Myc pathway.SNORD89 通过调控 Notch1-c-Myc 通路促进卵巢癌细胞干性表型。
卵巢癌干细胞综述：与高复发率的关联、潜在机制及治疗机遇
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