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DOI 10.1016/j.cellsig.2023.110748

Медицинская библиотека · Cellular signalling · 2023

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

Tang Yuting, Zhu Qinghai, Yang Li, Meng Ying, Zhang Gao, Zhou Tian, Wang Chenxing, Song Xiaomeng, Su Yu-Xiong, Ye Jinhai

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

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.

Для цитирования: Tang Yuting, Zhu Qinghai, Yang Li, Meng Ying, Zhang Gao, Zhou Tian, Wang Chenxing, Song Xiaomeng, Su Yu-Xiong, Ye Jinhai. MiR-200b-5p inhibits tumor progression in salivary adenoid cystic carcinoma via targeting BTBD1.. Cellular signalling. 2023. DOI: 10.1016/j.cellsig.2023.110748.

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