Department of Biology, Faculty of Arts and Sciences, American University of Beirut, Beirut, Lebanon.
Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Sci Rep. 2024 Oct 21;14(1):24711. doi: 10.1038/s41598-024-73632-0.
Although the miR-183/182/96 cluster is overexpressed in breast cancer (BC), little is known about its role in the development of pre-carcinogenic lesions which harbor disrupted adherens junctions (AJ) and may promote BC. Here, we used microRNA and RNA sequencing data from The Cancer Genome Atlas (TCGA) Breast Cancer project to investigate the relationship between the miR-183/182/96 cluster and AJ signaling in early-stage BC. We found that all members of the cluster are significantly overexpressed in early-stage BC, the AJ signaling pathway is enriched for genes down-regulated in early-stage BC, and the AJ signaling pathway is enriched for experimentally validated targets of the miR-183/182/96 cluster. The expression of hsa-miR-182 correlates inversely with the mRNA expression of four of its target genes belonging to the AJ signaling pathway: WASF3, EGFR, MET, and CTNNA3. However, the correlations between hsa-miR-182 and AJ gene expression did not differ significantly between targets and non-targets of hsa-miR-182. This suggests that regulatory effects of microRNAs are less pronounced in cancer, as has been shown by other studies. Furthermore, WASF3, EGFR, and MET are oncogenes that tend to be upregulated in later BC stages, implying that the role of some AJ genes changes with different BC stages.
尽管 miR-183/182/96 簇在乳腺癌 (BC) 中过表达,但对于其在具有破坏黏附连接 (AJ) 的癌前病变发展中的作用知之甚少,而这些病变可能促进了 BC 的发生。在这里,我们使用来自癌症基因组图谱 (TCGA) 乳腺癌项目的 microRNA 和 RNA 测序数据,研究了 miR-183/182/96 簇与早期 BC 中的 AJ 信号通路之间的关系。我们发现,该簇的所有成员在早期 BC 中均显著过表达,AJ 信号通路富集了在早期 BC 中下调的基因,并且 AJ 信号通路富集了 miR-183/182/96 簇的实验验证靶点。hsa-miR-182 的表达与 AJ 信号通路的四个靶基因的 mRNA 表达呈负相关: WASF3、EGFR、MET 和 CTNNA3。然而,hsa-miR-182 与 AJ 基因表达之间的相关性在靶基因和非靶基因之间没有显著差异。这表明,正如其他研究所示,microRNAs 的调节作用在癌症中不太明显。此外,WASF3、EGFR 和 MET 是在晚期 BC 中倾向于上调的癌基因,这意味着一些 AJ 基因的作用随着不同的 BC 阶段而变化。