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长链非编码RNA CYP4A22-AS1通过miR-205-5p/表皮调节素和miR-34c-5p/凋亡抑制蛋白2轴促进肺腺癌进展。

LncRNA CYP4A22-AS1 promotes the progression of lung adenocarcinoma through the miR-205-5p/EREG and miR-34c-5p/BCL-2 axes.

作者信息

Dong Liyao, Zhang Lin, Zhao Xinyun, Zou Hongling, Lin Sisi, Zhu Xinping, Cao Jili, Zhou Chun, Yu Zhihong, Zhu Yongqiang, Chai Kequn, Li Mingqian, Li Qun

机构信息

College of Life Science, Sichuan Normal University, Chengdu, 610101, Sichuan, China.

Zhejiang Provincial Key Laboratory of Cancer Prevention and Treatment Technology of Integrated Traditional Chinese and Western Medicine, Zhejiang Academy of Traditional Chinese Medicine, Tongde Hospital of Zhejiang Province, Hangzhou, 310012, Zhejiang, China.

出版信息

Cancer Cell Int. 2023 Sep 5;23(1):194. doi: 10.1186/s12935-023-03036-z.

DOI:10.1186/s12935-023-03036-z
PMID:37670265
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10478502/
Abstract

OBJECTIVES

Lung adenocarcinoma (LUAD) exhibits a higher fatality rate among all cancer types worldwide, yet the precise mechanisms underlying its initiation and progression remain unknown. Mounting evidence suggests that long non-coding RNAs (lncRNAs) exert significant regulatory roles in cancer development and progression. Nevertheless, the precise involvement of lncRNA CYP4A22-AS1 in LUAD remains incompletely comprehended.

METHODS

Bioinformatics analyses evaluated the expression level of CYP4A22-AS1 in lung adenocarcinoma and paracancer. The LUAD cell line with a high expression of CYP4A22-AS1 was constructed to evaluate the role of CYP4A22-AS1 in the proliferation and metastasis of LUAD by CCK8, scratch healing, transwell assays, and animal experiments. We applied transcriptome and microRNA sequencing to examine the mechanism of CYP4A22-AS1 enhancing the proliferation and metastasis of LUAD. Luciferase reporter gene analyses, west-blotting, and qRT-PCR were carried out to reveal the interaction between CYP4A22-AS1, miR-205-5p/EREG, and miR-34c-5p/BCL-2 axes.

RESULTS

CYP4A22-AS1 expression was significantly higher in LUAD tissues than in the adjacent tissues. Furthermore, we constructed a LUAD cell line with a high expression of CYP4A22-AS1 and noted that the high expression of CYP4A22-AS1 significantly enhanced the proliferation and metastasis of LUAD. We applied transcriptome and microRNA sequencing to examine the mechanism of CYP4A22-AS1 enhancing the proliferation and metastasis of LUAD. CYP4A22-AS1 increased the expression of EREG and BCL-2 by reducing the expression of miR-205-5p and miR-34-5p and activating the downstream signaling pathway of EGFR and the anti-apoptotic signaling pathway of BCL-2, thereby triggering the proliferation and metastasis of LUAD. The transfection of miR-205-5p and miR-34-5p mimics inhibited the role of CYP4A22-AS1 in enhancing tumor progression.

CONCLUSION

This study elucidates the molecular mechanism whereby CYP4A22-AS1 overexpression promotes LUAD progression through the miR-205-5p/EREG and miR-34c-5p/BCL-2 axes.

摘要

目的

肺腺癌（LUAD）在全球所有癌症类型中具有较高的死亡率，但其发生和发展的精确机制仍不清楚。越来越多的证据表明，长链非编码RNA（lncRNAs）在癌症发展和进程中发挥着重要的调控作用。然而，lncRNA CYP4A22-AS1在LUAD中的具体作用仍未完全明确。

方法

通过生物信息学分析评估CYP4A22-AS1在肺腺癌及癌旁组织中的表达水平。构建CYP4A22-AS1高表达的LUAD细胞系，采用CCK8、划痕愈合、Transwell实验及动物实验评估CYP4A22-AS1在LUAD增殖和转移中的作用。应用转录组和微小RNA测序检测CYP4A22-AS1促进LUAD增殖和转移的机制。通过荧光素酶报告基因分析、蛋白质免疫印迹法和定量逆转录聚合酶链反应揭示CYP4A22-AS1、miR-205-5p/EREG和miR-34c-5p/BCL-2轴之间的相互作用。

结果

CYP4A22-AS1在LUAD组织中的表达显著高于相邻组织。此外，我们构建了CYP4A22-AS1高表达的LUAD细胞系，并发现CYP4A22-AS1的高表达显著增强了LUAD的增殖和转移。我们应用转录组和微小RNA测序检测CYP4A22-AS1促进LUAD增殖和转移的机制。CYP4A22-AS1通过降低miR-205-5p和miR-34-5p的表达，激活EGFR下游信号通路和BCL-2抗凋亡信号通路，从而增加EREG和BCL-2的表达，进而引发LUAD的增殖和转移。转染miR-205-5p和miR-34-5p模拟物可抑制CYP4A22-AS1在促进肿瘤进展中的作用。

结论

本研究阐明了CYP4A22-AS1过表达通过miR-205-5p/EREG和miR-34c-5p/BCL-2轴促进LUAD进展的分子机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/5607293f9e02/12935_2023_3036_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/ae137c7e0fa7/12935_2023_3036_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/b99668c9eddb/12935_2023_3036_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/42ddfb61eb13/12935_2023_3036_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/27795f4d6d11/12935_2023_3036_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/d8a145416a32/12935_2023_3036_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/f16482f10414/12935_2023_3036_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/1a0c7353573b/12935_2023_3036_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/5607293f9e02/12935_2023_3036_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/ae137c7e0fa7/12935_2023_3036_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/b99668c9eddb/12935_2023_3036_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/42ddfb61eb13/12935_2023_3036_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/27795f4d6d11/12935_2023_3036_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/d8a145416a32/12935_2023_3036_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/f16482f10414/12935_2023_3036_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/1a0c7353573b/12935_2023_3036_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c4/10478502/5607293f9e02/12935_2023_3036_Fig3_HTML.jpg

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