Meng Yanchun, Tang Hao, Luo Zhiguo, Tan Wenlong, Chen Lin, Du Yiqun, Tao Zhonghua, Huang Mingzhu, Li Wenhua, Cao Jun, Wang Leiping, Li Ting, Liu Xin, Lv Fangfang, Liu Xiaojian, Zhang Jian, Zheng Lei, Hu Xichun
Department of Medical Oncology, Fudan University Shanghai Cancer Center, Shanghai, China.
Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, China.
Transl Cancer Res. 2021 Mar;10(3):1238-1248. doi: 10.21037/tcr-20-2681.
The microRNA (miRNA) miR-133a-1 has been identified as a tumor suppressor in breast cancer. However, the underlying mechanisms of miR-133a-1 in breast cancer have not been fully elucidated. This study aimed to explore the targets of miR-133a-1 in breast cancer using an integrated bioinformatics approach.
Human SKBR3 breast cancer cells were transfected with miR-133a-1 or a miRNA negative control (miRNA-NC) for 48 hours. The RNA-seq sequencing technique was performed to identify the differential expression of genes induced by miR-133a-1 overexpression. Functional enrichment analysis was conducted to determine the target genes and pathways involved in breast cancer.
Breast cancer patients with high levels of miR-133a-1 expression commonly showed longer overall survival compared to patients with a low level of miR-133a-1 expression. Using Cuffdiff, we identified 1,216 differentially expressed genes induced by miR-133a-1 overexpression, including 653 upregulated and 563 downregulated genes. was the most upregulated gene and was the most downregulated gene. The top 10 pathways related to the differentially expressed genes were identified through Gene Ontology (GO) enrichment analysis. Sex-determining region Y-box 9 () demonstrated the highest semantic similarities among the differentially expressed genes. Since and were hub nodes in the protein-protein interaction network, the gene may be a target of miR-133a-1 in breast cancer.
This report provides useful insights for understanding the underlying mechanisms in the pathogenesis of breast cancer.
微小RNA(miRNA)miR-133a-1已被确定为乳腺癌中的一种肿瘤抑制因子。然而,miR-133a-1在乳腺癌中的潜在机制尚未完全阐明。本研究旨在使用综合生物信息学方法探索miR-133a-1在乳腺癌中的靶标。
将miR-133a-1或微小RNA阴性对照(miRNA-NC)转染到人SKBR3乳腺癌细胞中48小时。采用RNA测序技术鉴定miR-133a-1过表达诱导的基因差异表达。进行功能富集分析以确定参与乳腺癌的靶基因和途径。
与miR-133a-1低表达患者相比,miR-133a-1高表达的乳腺癌患者通常总生存期更长。使用Cuffdiff,我们鉴定出1216个由miR-133a-1过表达诱导的差异表达基因,包括653个上调基因和563个下调基因。 是上调最显著的基因, 是下调最显著的基因。通过基因本体论(GO)富集分析确定了与差异表达基因相关的前10条途径。性别决定区Y盒9( )在差异表达基因中显示出最高的语义相似性。由于 和 在蛋白质-蛋白质相互作用网络中是枢纽节点, 基因可能是miR-133a-1在乳腺癌中的一个靶标。
本报告为理解乳腺癌发病机制的潜在机制提供了有用的见解。