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miR-30b-3p通过靶向调控COX6B1抑制肺腺癌细胞的增殖和侵袭

BACKGROUND AND OBJECTIVE: Lung adenocarcinoma (LUAD) is the most common clinical histological subtype of lung cancer and microRNAs (miRNAs) are a type of small non-coding RNAs which play a central role in cells. miR-30b-3p plays a key effect in many types of carcinoma, but there is still very little...

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Formato: Online Artículo Texto
Lenguaje:English
Publicado: 中国肺癌杂志编辑部 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9411956/
https://www.ncbi.nlm.nih.gov/pubmed/36002193
http://dx.doi.org/10.3779/j.issn.1009-3419.2022.101.42
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description BACKGROUND AND OBJECTIVE: Lung adenocarcinoma (LUAD) is the most common clinical histological subtype of lung cancer and microRNAs (miRNAs) are a type of small non-coding RNAs which play a central role in cells. miR-30b-3p plays a key effect in many types of carcinoma, but there is still very little research on how it works in lung adenocarcinoma. The role and mechanism of miR-30b-3p in the proliferation and invasion of LUAD were explored in this study, to provide new targets for inhibiting the proliferation and invasion of LUAD. METHODS: NCBI database was used to screen out miRNA with obvious differential expression, and the differential expression and survival curve were searched by StarBase database. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression of miR-30b-3p in each lung adenocarcinoma cell line. 5-ethynyl-2'-deoxyuridine (EdU) cell proliferation assay and Transwell invasion assay were used to detect the proliferation and invasion of A549 cells in each group. The target genes of miR-30b-3p were determined by the target gene prediction websites. Western blot assay was used to detect the expression of COX6B1 in each group of A549 cells. Double luciferase assay was used to verify the targeted binding relationship between miR-30b-3p and COX6B1. RESULTS: The expression of miR-30b-3p in lung adenocarcinoma tissues and lung adenocarcinoma cells was downregulated (P<0.05). Low expression levels of miR-30b-3p were associated with poor prognosis in patients with lung adenocarcinoma (P=0.005,8). Overexpression of miR-30b-3p could inhibit the proliferation and the invasion of lung adenocarcinoma cells (P<0.05). Double luciferase assay proved that miR-30b-3p could target and bind to COX6B1 (P<0.05). Western blot analysis showed that the overexpression of miR-30b-3p could downregulate the expression of COX6B1 in A549 cells (P<0.05). EdU cell proliferation assay and Transwell invasion assay showed that the overexpression of miR-30b-3p could reverse the promoting effect of upregulation of COX6B1 on proliferation and invasion in lung adenocarcinoma cells (P<0.05). CONCLUSION: miR-30b-3p acts as a tumor suppressor gene in lung adenocarcinoma, and it can inhibit the proliferation and invasion of lung adenocarcinoma by targeting the expression of COX6B1.
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spelling pubmed-94119562022-09-12 miR-30b-3p通过靶向调控COX6B1抑制肺腺癌细胞的增殖和侵袭 Zhongguo Fei Ai Za Zhi 基础研究 BACKGROUND AND OBJECTIVE: Lung adenocarcinoma (LUAD) is the most common clinical histological subtype of lung cancer and microRNAs (miRNAs) are a type of small non-coding RNAs which play a central role in cells. miR-30b-3p plays a key effect in many types of carcinoma, but there is still very little research on how it works in lung adenocarcinoma. The role and mechanism of miR-30b-3p in the proliferation and invasion of LUAD were explored in this study, to provide new targets for inhibiting the proliferation and invasion of LUAD. METHODS: NCBI database was used to screen out miRNA with obvious differential expression, and the differential expression and survival curve were searched by StarBase database. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression of miR-30b-3p in each lung adenocarcinoma cell line. 5-ethynyl-2'-deoxyuridine (EdU) cell proliferation assay and Transwell invasion assay were used to detect the proliferation and invasion of A549 cells in each group. The target genes of miR-30b-3p were determined by the target gene prediction websites. Western blot assay was used to detect the expression of COX6B1 in each group of A549 cells. Double luciferase assay was used to verify the targeted binding relationship between miR-30b-3p and COX6B1. RESULTS: The expression of miR-30b-3p in lung adenocarcinoma tissues and lung adenocarcinoma cells was downregulated (P<0.05). Low expression levels of miR-30b-3p were associated with poor prognosis in patients with lung adenocarcinoma (P=0.005,8). Overexpression of miR-30b-3p could inhibit the proliferation and the invasion of lung adenocarcinoma cells (P<0.05). Double luciferase assay proved that miR-30b-3p could target and bind to COX6B1 (P<0.05). Western blot analysis showed that the overexpression of miR-30b-3p could downregulate the expression of COX6B1 in A549 cells (P<0.05). EdU cell proliferation assay and Transwell invasion assay showed that the overexpression of miR-30b-3p could reverse the promoting effect of upregulation of COX6B1 on proliferation and invasion in lung adenocarcinoma cells (P<0.05). CONCLUSION: miR-30b-3p acts as a tumor suppressor gene in lung adenocarcinoma, and it can inhibit the proliferation and invasion of lung adenocarcinoma by targeting the expression of COX6B1. 中国肺癌杂志编辑部 2022-08-20 /pmc/articles/PMC9411956/ /pubmed/36002193 http://dx.doi.org/10.3779/j.issn.1009-3419.2022.101.42 Text en 版权所有©《中国肺癌杂志》编辑部2022 https://creativecommons.org/licenses/by/3.0/This is an open access article distributed in accordance with the terms of the Creative Commons Attribution (CC BY 3.0) License. See: https://creativecommons.org/licenses/by/3.0/.
spellingShingle 基础研究
miR-30b-3p通过靶向调控COX6B1抑制肺腺癌细胞的增殖和侵袭
title miR-30b-3p通过靶向调控COX6B1抑制肺腺癌细胞的增殖和侵袭
title_full miR-30b-3p通过靶向调控COX6B1抑制肺腺癌细胞的增殖和侵袭
title_fullStr miR-30b-3p通过靶向调控COX6B1抑制肺腺癌细胞的增殖和侵袭
title_full_unstemmed miR-30b-3p通过靶向调控COX6B1抑制肺腺癌细胞的增殖和侵袭
title_short miR-30b-3p通过靶向调控COX6B1抑制肺腺癌细胞的增殖和侵袭
title_sort mir-30b-3p通过靶向调控cox6b1抑制肺腺癌细胞的增殖和侵袭
topic 基础研究
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9411956/
https://www.ncbi.nlm.nih.gov/pubmed/36002193
http://dx.doi.org/10.3779/j.issn.1009-3419.2022.101.42
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