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Article: MiR-200b-5p inhibits tumor progression in salivary adenoid cystic carcinoma via targeting BTBD1

TitleMiR-200b-5p inhibits tumor progression in salivary adenoid cystic carcinoma via targeting BTBD1
Authors
KeywordsBTBD1
miR-200b-5p
PI3K/AKT
Salivary adenoid cystic carcinoma (SACC)
Tumor progression
Issue Date1-Sep-2023
PublisherElsevier
Citation
Cellular Signalling, 2023, v. 109 How to Cite?
Abstract

Salivary adenoid cystic carcinoma (SACC) is a rare malignant tumor of the salivary gland. Studies have suggested that miRNA may play a crucial role in the invasion and metastasis of SACC. This study aimed to investigate the role of miR-200b-5p in SACC progression. Reverse transcription-quantitative PCR and western blot assay were used to detect the expression levels of miR-200b-5p and BTBD1. The biological functions of miR-200b-5p were evaluated via wound-healing assays, transwell assays, and xenograft nude mice model. The interaction between miR-200b-5p and BTBD1 was assessed using luciferase assay. Results showed that miR-200b-5p was downregulated in the SACC tissues while BTBD1 was upregulated. miR-200b-5p overexpression suppressed SACC cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Bioinformatics prediction and luciferase reporter assay revealed that miR-200b-5p could directly bind to BTBD1. Besides, miR-200b-5p overexpression could rescue the tumor-promoting effect of BTBD1. miR-200b-5p inhibited tumor progression by modulating EMT-related proteins, targeting BTBD1 and inhibiting PI3K/AKT signaling pathway. Overall, our findings indicate that miR-200b-5p can suppress SACC proliferation, migration, invasion, and EMT by regulating BTBD1 and PI3K/AKT axis, providing a promising therapeutic target for SACC treatment.


Persistent Identifierhttp://hdl.handle.net/10722/331509
ISSN
2021 Impact Factor: 4.850
2020 SCImago Journal Rankings: 1.435
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorTang, Yuting-
dc.contributor.authorZhu, Qinghai-
dc.contributor.authorYang, Li-
dc.contributor.authorMeng, Ying-
dc.contributor.authorZhang, Gao-
dc.contributor.authorZhou, Tian-
dc.contributor.authorWang, Chenxing-
dc.contributor.authorSong, Xiaomeng-
dc.contributor.authorSu, Yu-Xiong-
dc.contributor.authorYe, Jinhai-
dc.date.accessioned2023-09-21T06:56:29Z-
dc.date.available2023-09-21T06:56:29Z-
dc.date.issued2023-09-01-
dc.identifier.citationCellular Signalling, 2023, v. 109-
dc.identifier.issn0898-6568-
dc.identifier.urihttp://hdl.handle.net/10722/331509-
dc.description.abstract<p>Salivary adenoid cystic carcinoma (SACC) is a rare malignant tumor of the salivary gland. Studies have suggested that miRNA may play a crucial role in the invasion and metastasis of SACC. This study aimed to investigate the role of miR-200b-5p in SACC progression. Reverse transcription-quantitative PCR and <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/western-blot" title="Learn more about western blot from ScienceDirect's AI-generated Topic Pages">western blot</a> assay were used to detect the expression levels of miR-200b-5p and <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/btb-poz-domain" title="Learn more about BTBD1 from ScienceDirect's AI-generated Topic Pages">BTBD1</a>. The biological functions of miR-200b-5p were evaluated via wound-healing assays, transwell assays, and xenograft <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/nude-mouse" title="Learn more about nude mice from ScienceDirect's AI-generated Topic Pages">nude mice</a> model. The interaction between miR-200b-5p and <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/btb-poz-domain" title="Learn more about BTBD1 from ScienceDirect's AI-generated Topic Pages">BTBD1</a> was assessed using <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/luciferase" title="Learn more about luciferase from ScienceDirect's AI-generated Topic Pages">luciferase</a> assay. Results showed that miR-200b-5p was downregulated in the SACC tissues while BTBD1 was upregulated. miR-200b-5p overexpression suppressed SACC <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/cell-proliferation" title="Learn more about cell proliferation from ScienceDirect's AI-generated Topic Pages">cell proliferation</a>, migration, invasion, and epithelial-mesenchymal transition (EMT). Bioinformatics prediction and <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/luciferase" title="Learn more about luciferase from ScienceDirect's AI-generated Topic Pages">luciferase</a> reporter assay revealed that miR-200b-5p could directly bind to BTBD1. Besides, miR-200b-5p overexpression could rescue the tumor-promoting effect of BTBD1. miR-200b-5p inhibited tumor progression by modulating EMT-related proteins, targeting BTBD1 and inhibiting PI3K/AKT <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/signal-transduction" title="Learn more about signaling pathway from ScienceDirect's AI-generated Topic Pages">signaling pathway</a>. Overall, our findings indicate that miR-200b-5p can suppress SACC proliferation, migration, invasion, and EMT by regulating BTBD1 and PI3K/AKT axis, providing a promising therapeutic target for SACC treatment.</p>-
dc.languageeng-
dc.publisherElsevier-
dc.relation.ispartofCellular Signalling-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectBTBD1-
dc.subjectmiR-200b-5p-
dc.subjectPI3K/AKT-
dc.subjectSalivary adenoid cystic carcinoma (SACC)-
dc.subjectTumor progression-
dc.titleMiR-200b-5p inhibits tumor progression in salivary adenoid cystic carcinoma via targeting BTBD1-
dc.typeArticle-
dc.identifier.doi10.1016/j.cellsig.2023.110748-
dc.identifier.scopuseid_2-s2.0-85161657107-
dc.identifier.volume109-
dc.identifier.isiWOS:001027069700001-
dc.identifier.issnl0898-6568-

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