miR-19a-3p accelerates the development of melanoma and reduces the prognosis of patients
Previous studies have shown that miR-19a-3p is expressed at higher levels in melanoma tissues, suggesting that it may be involved in the progression of melanoma. This study sought to elucidate the biological function of miR-19a-3p in melanoma. In this study, RT-qPCR was performed to measure the expression level of miR-19a-3p in melanoma tissues and cell lines. The relationship between miR-19a-3p and the prognosis of melanoma patients was assessed by Kaplan-Meier analysis and the Cox regression model. The effects of miR-19a-3p on cell proliferation, migration, and invasion were analyzed by Cell Counting Kit-8 (CCK-8) and Transwell assays. The targeting relationship between miR-19a-3p and adrenergic receptor β1 (ADRB1) was verified by Dual-luciferase reporter assay. miR-19a-3p was significantly overexpressed in melanoma tissues and cell lines. The high expression of miR-19a-3p was significantly associated with a higher TNM stage, lymph node metastasis, and decreased survival rate. Inhibition of miR-19a-3p could significantly weaken the proliferation, migration, and invasion abilities of melanoma cells. ADRB1 was a direct target of miR-19a-3p, and their expressions were negatively correlated. Knockdown of ADRB1 reversed the anti-tumor effect of miR-19a-3p inhibitor. miR-19a-3p promoted the malignant progression of melanoma by targeting and inhibiting ADRB1. Its expression level can serve as an independent biomarker for evaluating the prognosis of melanoma patients.
Authors
- Guanghui Wang (ORCID: https://orcid.org/0000-0001-6213-0693)
- Liwei Xu
- Ting Kang (ORCID: https://orcid.org/0000-0002-5046-2399)
Institutions
- Gansu Provincial Maternal and Child Health Hospital (CN)
- Lanzhou University Second Hospital (CN)
- Lanzhou University (CN)
Publication Details
- Journal
- World Journal of Surgical Oncology
- Published
- 2026-02-04
- DOI
- https://doi.org/10.1186/s12957-026-04226-5
- Primary Topic
- Cancer, Stress, Anesthesia, and Immune Response
- Type
- article
- Field-Weighted Citation Impact
- 0.00