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长链非编码 RNA FAM83A 反义 RNA 1（lncRNA FAM83A-AS1）靶向 microRNA-141-3p 调控肺腺癌细胞增殖、迁移、侵袭和上皮间质转化进展。

Long non-coding RNA FAM83A antisense RNA 1 (lncRNA FAM83A-AS1) targets microRNA-141-3p to regulate lung adenocarcinoma cell proliferation, migration, invasion, and epithelial-mesenchymal transition progression.

机构信息

Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.

Department of the Bone and Joint Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, China.

出版信息

Bioengineered. 2022 Mar;13(3):4964-4977. doi: 10.1080/21655979.2022.2037871.

DOI:10.1080/21655979.2022.2037871
PMID:35164653
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8973779/
Abstract

The current paper investigates how long non-coding RNA (lncRNA) FAM83A antisense RNA 1 (lncRNA FAM83A-AS1) affected the epithelial-mesenchymal transformation (EMT), growth, invasion and migration of lung adenocarcinoma (LUAD) via targeting miRNA-141-3p. The GEPIA and ENCORI databases were used to analyze differences in lncRNA FAM83A-AS1 levels within LUAD samples. FAM83A-AS1 and miR-141-3p levels were assessed using qRT-PCR among 30 LUAD samples and surrounding normal tissues. In addition, we analyzed how FAM83A-AS1 affected proliferation, invasion, migration, and EMT processes of LUAD cells by targeting miR-141-3p through EdU, CCK-8 assay, scratch assay, transwell migration and invasion assay, immunofluorescence (IF) staining and WB assay. MicroRNAs targeting FAM83A-AS1 were screened using AnnoLnc2 and identified by RT-qPCR. Dual-luciferase assays were utilized to evaluate the connection between FAM83A-AS1 and miR-141-3p. FAM83A-AS1 expression was remarkably raised in lung cancer cells and tissue samples; however, miR-141-3p level markedly reduced relative to healthy samples. FAM83A-AS1 silencing suppressed EMT, growth, invasion and migration of LUAD cells. MiR-141-3p was the possible FAM83A-AS1 binding target negatively associated with FAM83A-AS1. The miR-141-3p inhibitor partly abolished the FAM83A-AS1 knockdown-induced inhibition on EMT, cell growth, invasion and migration in LUAD cells. In addition, miR-141-3p down-regulation abolished the inhibition of E-box-bound zinc finger protein 1 and 2 protein production following FAM83A-AS1 knockdown. According to our results, FAM83A-AS1/miR-141-3p axis plays an important role in LUAD occurrence and development. FAM83A-AS1 sponged miR-141-3p to down-regulate the level of the latter within LUAD and thereby encouraging LUAD development and suggesting a possible novel therapeutic approach for LUAD.

摘要

本文研究了长非编码 RNA (lncRNA) FAM83A 反义 RNA 1 (lncRNA FAM83A-AS1) 如何通过靶向 miRNA-141-3p 影响肺腺癌 (LUAD) 的上皮-间充质转化 (EMT)、生长、侵袭和迁移。使用 GEPIA 和 ENCORI 数据库分析 LUAD 样本中 lncRNA FAM83A-AS1 水平的差异。在 30 个 LUAD 样本和周围正常组织中使用 qRT-PCR 评估 FAM83A-AS1 和 miR-141-3p 的水平。此外，我们通过 EdU、CCK-8 测定、划痕测定、transwell 迁移和侵袭测定、免疫荧光 (IF) 染色和 WB 测定，分析 FAM83A-AS1 通过靶向 miR-141-3p 如何影响 LUAD 细胞的增殖、侵袭、迁移和 EMT 过程。使用 AnnoLnc2 筛选靶向 FAM83A-AS1 的 microRNAs，并通过 RT-qPCR 进行鉴定。双荧光素酶测定用于评估 FAM83A-AS1 与 miR-141-3p 之间的联系。FAM83A-AS1 在肺癌细胞和组织样本中表达显著升高，而与健康样本相比，miR-141-3p 水平明显降低。FAM83A-AS1 沉默抑制 LUAD 细胞的 EMT、生长、侵袭和迁移。miR-141-3p 是 FAM83A-AS1 负相关的可能结合靶标。miR-141-3p 抑制剂部分消除了 FAM83A-AS1 敲低对 LUAD 细胞 EMT、细胞生长、侵袭和迁移的抑制作用。此外，FAM83A-AS1 敲低后，E-盒结合锌指蛋白 1 和 2 蛋白的产生被抑制，miR-141-3p 下调消除了这种抑制作用。根据我们的结果，FAM83A-AS1/miR-141-3p 轴在 LUAD 的发生和发展中起重要作用。FAM83A-AS1 吸附 miR-141-3p，降低后者在 LUAD 中的水平，从而促进 LUAD 的发展，并为 LUAD 提供一种新的可能的治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/53924216c29e/KBIE_A_2037871_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/6a1319583010/KBIE_A_2037871_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/3d98214435bc/KBIE_A_2037871_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/24c2c5454266/KBIE_A_2037871_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/0c7c798d8ef0/KBIE_A_2037871_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/6ae9cf8750d7/KBIE_A_2037871_F0004a_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/1967705cbc62/KBIE_A_2037871_F0004b_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/53924216c29e/KBIE_A_2037871_F0005_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/6a1319583010/KBIE_A_2037871_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/3d98214435bc/KBIE_A_2037871_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/24c2c5454266/KBIE_A_2037871_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/0c7c798d8ef0/KBIE_A_2037871_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/6ae9cf8750d7/KBIE_A_2037871_F0004a_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/1967705cbc62/KBIE_A_2037871_F0004b_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/80c9/8973779/53924216c29e/KBIE_A_2037871_F0005_OC.jpg

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