lncRNA SEMA3B-AS1 Inhibits miR-513c-5p to Regulate the Progression of Triple-negative Breast Cancer.
Anticancer Res
; 43(12): 5475-5484, 2023 Dec.
Article
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| MEDLINE
| ID: mdl-38030196
ABSTRACT
BACKGROUND/AIM:
Triple-negative breast cancer (TNBC) is the most malignant breast cancer subtype with a short survival time and high morality. There is an urgent need for effective indicators able to predict tumor progression and provide reference for adjusting the therapeutic strategy of TNBC. lncRNA semaphorin 3B antisense RNA1-AS1 (SEMA3B-AS1) was previously identified to be correlated with the stemness and autophagy of breast cancer. SEMA3B-AS1's role in TNBC was investigated in the present study, aiming to explore a novel biomarker for the development and prognosis of TNBC. MATERIALS ANDMETHODS:
SEMA3B-AS1 expression was detected in tissue samples from 113 TNBC patients using PCR. The clinical significance of SEMA3B-AS1 was assessed by the Chi-square test and Cox analysis. The in vitro function of SEMA3B-AS1 was investigated by CCK8 and Transwell assay. Study of molecular mechanism, correlation analysis and dual-luciferase reporter assay were employed to assess the correlation of SEMA3B-AS1 with miR-513c-5p.RESULTS:
A significant down-regulation of SEMA3B-AS1 was observed in TNBC, which was related to patient TNM stage, lymph node metastasis, and Ki67 levels. SEMA3B-AS1 down-regulation indicated patients' adverse prognoses and served as an independent prognostic factor. In vitro, SEMA3B-AS1 suppressed the stemness, proliferation, and metastasis of TNBC cells. Moreover, SEMA3B-AS1 negatively regulated miR-513c-5p, which could reverse the inhibitory effects of SEMA3B-AS1 on TNBC cells.CONCLUSION:
SEM3B-AS1 indicates the severity of TNBC patients and regulates tumor progression via modulating miR-513c-5p.Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Semaforinas
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MicroARNs
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ARN Largo no Codificante
/
Neoplasias de la Mama Triple Negativas
Límite:
Humans
Idioma:
En
Revista:
Anticancer Res
Año:
2023
Tipo del documento:
Article