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miR-125b prevent the progression of esophageal squamous cell carcinoma through the p38-MAPK signaling pathway.
Cheng, Chun; Mao, Qinghua; Shi, Minxin; Lu, Haimin; Shen, Biao; Xiao, Ting; Yang, Aimin; Liu, Yupeng.
Afiliação
  • Cheng C; Department of Thoracic Surgery, Affiliated Tumor Hospital Nantong University, Nantong, China.
  • Mao Q; Department of Thoracic Surgery, Affiliated Tumor Hospital Nantong University, Nantong, China.
  • Shi M; Department of Thoracic Surgery, Affiliated Tumor Hospital Nantong University, Nantong, China.
  • Lu H; Department of Thoracic Surgery, Affiliated Tumor Hospital Nantong University, Nantong, China.
  • Shen B; Department of Thoracic Surgery, Affiliated Tumor Hospital Nantong University, Nantong, China.
  • Xiao T; Department of Thoracic Surgery, Affiliated Tumor Hospital Nantong University, Nantong, China.
  • Yang A; Department of Thoracic Surgery, Affiliated Tumor Hospital Nantong University, Nantong, China.
  • Liu Y; Department of Thoracic Surgery, Affiliated Tumor Hospital Nantong University, Nantong, China.
J Gastrointest Oncol ; 11(6): 1113-1122, 2020 Dec.
Article em En | MEDLINE | ID: mdl-33456986
ABSTRACT

BACKGROUND:

To examine the clinical significance of miR-125b in esophageal squamous cell carcinoma (ESCC) and to research the effect of miR-125b on the biological function of ESCC cells and the relevant underlying mechanism.

METHODS:

The expression of miR-125b in ESCC tissues and cell lines were discovered by RT-PCR assay. The interrelation between miR-125b expression and clinicopathological parameters and the forecasting of ESCC patients were analyzed. CCK-8 method and Transwell methods were used to detect the increased growth, shifting, and irruption of ESCC cells. Bioinformatics analysis was applied to forecast the possible target genes of miR-125b and verified through dual-luciferase reporter gene assay. After that, the expression of p38-MAPK mRNA and protein were found out by RT-PCR and Western blot.

RESULTS:

The expression of miR-125b was down-regulated in ESCC tissues and cell lines (P<0.05). And the expression of miR-125b was closely about tumor differentiation, TNM level, and lymph node metastasis in ESCC patients. The low miR-125b formulation was closely related to rough forecasting in ESCC patients. Large scale expression of miR-125b can effectively decrease the acceleration, shifting, and irrupting strengths of ESCC cells. Bioinformatics analysis showed p38-MAPK was forecasted to be a potential mark of miR-125b, which was confirmed by dual luciferase assay, and extreme expression of miR-125b can stop the expression of p38-MAPK mRNA and protein.

CONCLUSIONS:

miR-125b is down-regulated in ESCC. Moreover, its expression level is significant concerning tumor progression and prognosis in patients with ESCC. MiR-125b can stop the high growth and shifting of ESCC cells having p38-MAPK at target.
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Texto completo: 1 Coleções: 01-internacional Temas: Geral Base de dados: MEDLINE Idioma: En Revista: J Gastrointest Oncol Ano de publicação: 2020 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Coleções: 01-internacional Temas: Geral Base de dados: MEDLINE Idioma: En Revista: J Gastrointest Oncol Ano de publicação: 2020 Tipo de documento: Article País de afiliação: China