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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
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/ce7795cf3fed/cells-12-01885-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/eb0e1e6c35aa/cells-12-01885-g002.jpg
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
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/7835d0c79550/cells-12-01885-g005.jpg
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
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/ce7795cf3fed/cells-12-01885-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/eb0e1e6c35aa/cells-12-01885-g002.jpg
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
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3109/10378275/7835d0c79550/cells-12-01885-g005.jpg
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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[4]
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[5]
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[6]
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[7]
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本文引用的文献

[1]
MiR-202-3p inhibits the proliferation and metastasis of lung adenocarcinoma cells by targeting RRM2.

Ann Transl Med. 2022-12

[2]
MicroRNA signature of small-cell lung cancer after treatment failure: impact on oncogenic targets by miR-30a-3p control.

Mol Oncol. 2023-2

[3]
Salivary Exosomal MicroRNA-486-5p and MicroRNA-10b-5p in Oral and Oropharyngeal Squamous Cell Carcinoma.

Medicina (Kaunas). 2022-10-18

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Cells. 2022-8-13

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Anesthetic propofol enhances cisplatin-sensitivity of non-small cell lung cancer cells through N6-methyladenosine-dependently regulating the miR-486-5p/RAP1-NF-κB axis.

BMC Cancer. 2022-7-14

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Circular RNA EPB41 expression predicts unfavorable prognoses in NSCLC by regulating miR-486-3p/eIF5A axis-mediated stemness.

Cancer Cell Int. 2022-6-20

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Circ_CSPP1 Regulates the Development of Non-small Cell Lung Cancer via the miR-486-3p/BRD9 Axis.

Biochem Genet. 2023-2

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MiR-486-5p specifically suppresses SAPCD2 expression, which attenuates the aggressive phenotypes of lung adenocarcinoma cells.

Histol Histopathol. 2022-9

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A pan-cancer analysis of GINS complex subunit 4 to identify its potential role as a biomarker in multiple human cancers.

Am J Cancer Res. 2022-3-15

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