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肿瘤抑制基因和靶向基因的分子发病机制：促进肺腺癌的侵袭性。

The Molecular Pathogenesis of Tumor-Suppressive and Target Genes: Facilitates Aggressiveness in Lung Adenocarcinoma.

机构信息

Department of Pulmonary Medicine, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima 890-8544, Japan.

Department of Functional Genomics, Chiba University Graduate School of Medicine, Chuo-ku, Chiba 260-8670, Japan.

出版信息

Cells. 2023 Jul 18;12(14):1885. doi: 10.3390/cells12141885.

DOI:10.3390/cells12141885
PMID:37508549
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10378275/
Abstract

The involvement of passenger strands of miRNAs in the molecular pathogenesis of human cancers is a recent concept in miRNA research, and it will broaden our understanding of the molecular mechanisms of miRNA-mediated cancer. The analysis of our miRNA signature of LUAD revealed that both strands of pre- ( and ) were downregulated in LUAD tissues. Ectopic expression of both miRNAs induced cell cycle arrest in LUAD cells, suggesting both strands of miRNAs derived from pre- were tumor suppressive. Our in silico analysis showed a total of 99 genes may be under the control of both miRNAs in LUAD cells. Importantly, among these targets, the high expression of seven genes (, , , , , , and ) predicted a poorer prognosis of LUAD patients ( < 0.05). We focused on , a DNA replication complex GINS protein that plays an essential role in the initiation of DNA replication. Our functional assays showed that was directly controlled by both strands of pre-, and its aberrant expression facilitated the aggressive behavior of LUAD cells. is attractive as a therapeutic target for this disease. MiRNA analysis, including passenger strands, will further improve our understanding of the molecular pathogenesis of LUAD.

摘要

miRNA 乘客链参与人类癌症的分子发病机制是 miRNA 研究中的一个新概念，它将拓宽我们对 miRNA 介导的癌症的分子机制的理解。我们对 LUAD 的 miRNA 特征分析表明，pre-（和）的两条链在 LUAD 组织中均下调。这两种 miRNA 的异位表达诱导 LUAD 细胞周期停滞，表明源自 pre-的两条 miRNA 链均具有肿瘤抑制作用。我们的计算机分析显示，共有 99 个基因可能受 LUAD 细胞中这两种 miRNA 的控制。重要的是，在这些靶基因中，七种基因（，，，，，，和）的高表达预示着 LUAD 患者的预后较差（<0.05）。我们专注于，它是 DNA 复制复合物 GINS 蛋白，在 DNA 复制的起始中发挥重要作用。我们的功能测定表明，是由 pre-的两条链直接控制的，其异常表达促进了 LUAD 细胞的侵袭行为。作为这种疾病的治疗靶点很有吸引力。miRNA 分析，包括乘客链，将进一步提高我们对 LUAD 分子发病机制的理解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/e84c7c1dd865/cells-12-01885-g010.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/6f5058c99a97/cells-12-01885-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/e9c6515223aa/cells-12-01885-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/89c30f921c39/cells-12-01885-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/e84c7c1dd865/cells-12-01885-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/ce7795cf3fed/cells-12-01885-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/113b124136e9/cells-12-01885-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/33694efc6fa9/cells-12-01885-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/5c6116662191/cells-12-01885-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/6f5058c99a97/cells-12-01885-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/e9c6515223aa/cells-12-01885-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/89c30f921c39/cells-12-01885-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/e84c7c1dd865/cells-12-01885-g010.jpg

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