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

Cell Signal

Jiangsu Key Laboratory of Oral Disease, Jiangsu Province Engineering Research Center of Stomatological Translational Medicine, Nanjing Medical University, Nanjing 210029, China; Department of Oral and Maxillofacial Surgery, The Affiliated Stomatological Hospital of Nanjing Medical University, Nanjing 210029, China. Electronic address:

Published: September 2023

AI Article Synopsis

  • Salivary adenoid cystic carcinoma (SACC) is a rare salivary gland tumor linked to miRNA involvement in its progression, particularly focusing on miR-200b-5p.
  • Research found that miR-200b-5p levels were lower in SACC tissues while BTBD1 levels were higher; miR-200b-5p overexpression reduced cancer cell activities like proliferation and invasion.
  • The study suggests that miR-200b-5p functions by targeting BTBD1 and regulating the PI3K/AKT signaling pathway, indicating its potential as a therapeutic target for SACC treatment.

Article 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.

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Source
http://dx.doi.org/10.1016/j.cellsig.2023.110748DOI Listing

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