Oral diseases · 2021
miR-5191 acts as a tumor suppressor in salivary adenoid cystic carcinoma by targeting Notch-2.
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Li Zhi, Zhang Qian, Su Han, Li Hu-Yue, Cao Gang, Xu Jin-Ke, Wang Jun-Lan, Niu Chun-Zi, Zhang Feimin, Yang Jian, Chen Wei
Аннотация
OBJECTIVE: This study sought to investigate the effect of miR-5191 on proliferation, invasion and metastasis in salivary adenoid cystic carcinoma (SACC).
MATERIALS AND METHODS: The differential expression level of miR-5191 between 5 primary tumor and adjacent non-neoplastic samples, and in two SACC cell lines was detected by quantitative real-time PCR. Cell proliferation, invasion, and migration were performed, followed by luciferase reporter assay and western analysis. The effect of miR-5191 on cell proliferation and apoptosis was evaluated by cell growth and apoptosis assay. The function of miR-5191 in SACC tumorigenesis and metastasis in vivo was investigated by nude mice experiment. The associations between miR-5191/Notch-2 expression and clinicopathological features were analyzed.
RESULTS: miR-5191 was downregulated in primary tumor tissues and SACC-LM cells. By targeting Notch-2, miR-5191 expression level affected the migration, invasion, and proliferation of SACC cells. Overexpression of miR-5191 inhibited the expression levels of Notch-2, followed by the decreased expression of c-Myc, Bcl-2, Hes-1, Hey-1, and Cyclin D1. In vivo, miR-5191 overexpression suppressed the SACC tumorigenesis and pulmonary metastasis in mice. In SACC patients, higher expression of miR-5191 was related to better prognoses and lower possibility of metastasis.
CONCLUSIONS: miR-5191 acts as a tumor suppressor in SACC by targeting Notch-2.
MATERIALS AND METHODS: The differential expression level of miR-5191 between 5 primary tumor and adjacent non-neoplastic samples, and in two SACC cell lines was detected by quantitative real-time PCR. Cell proliferation, invasion, and migration were performed, followed by luciferase reporter assay and western analysis. The effect of miR-5191 on cell proliferation and apoptosis was evaluated by cell growth and apoptosis assay. The function of miR-5191 in SACC tumorigenesis and metastasis in vivo was investigated by nude mice experiment. The associations between miR-5191/Notch-2 expression and clinicopathological features were analyzed.
RESULTS: miR-5191 was downregulated in primary tumor tissues and SACC-LM cells. By targeting Notch-2, miR-5191 expression level affected the migration, invasion, and proliferation of SACC cells. Overexpression of miR-5191 inhibited the expression levels of Notch-2, followed by the decreased expression of c-Myc, Bcl-2, Hes-1, Hey-1, and Cyclin D1. In vivo, miR-5191 overexpression suppressed the SACC tumorigenesis and pulmonary metastasis in mice. In SACC patients, higher expression of miR-5191 was related to better prognoses and lower possibility of metastasis.
CONCLUSIONS: miR-5191 acts as a tumor suppressor in SACC by targeting Notch-2.