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Hsa-miR-1269a up-regulation fosters the malignant progression of esophageal squamous cell carcinoma via targeting FAM46C
被引:1
|作者:
Ma, Yuefeng
[1
]
Xing, Xin
[2
]
Cheng, Chuantao
[3
]
Kong, Ranran
[1
]
Sun, Liangzhang
[1
]
Zhao, Feng
[1
]
Zhang, Danjie
[1
]
Li, Jianzhong
[1
,4
]
机构:
[1] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Thorac Surg, Xian 710004, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Hlth Care Cadres, Xian 710004, Shaanxi, Peoples R China
[3] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Dermatol, Xian 710004, Shaanxi, Peoples R China
[4] Xi An Jiao Tong Univ, Affiliated Hosp 2, Dept Thorac Surg, 157 Xiwu Lu, Xian 710004, Shaanxi, Peoples R China
来源:
关键词:
Esophageal squamous cell carcinoma;
Hsa-miR-1269a;
FAM46C;
Proliferation;
Migration;
Invasion;
Apoptosis;
CANCER;
MICRORNAS;
PROTEINS;
PROMOTES;
D O I:
10.1016/j.mrfmmm.2023.111832
中图分类号:
Q81 [生物工程学(生物技术)];
Q93 [微生物学];
学科分类号:
071005 ;
0836 ;
090102 ;
100705 ;
摘要:
Esophageal squamous cell carcinoma (ESCC) is a malignancy of the alimentary tract resulting in death world-wide. The role and underlying mechanism of hsa-miR-1269a in the progression of ESCC remain unclear. In this study, hsa-miR-1269a was screened by differential expression analysis in TCGA, and its target gene FAM46C was predicted. qRT-PCR was conducted to assay the expression of hsa-miR-1269a and FAM46C in ESCC cells. The results showed that hsa-miR-1269a was upregulated in ESCC tissues and cell lines. Hsa-miR-1269a over -expression stimulated the proliferation, migration, and invasion capacities of ESCC cells, and FAM46C over -expression inhibited these phenotypes. Dual-luciferase assay verified that hsa-miR-1269a could target FAM46C. Next, qRT-PCR and western blot demonstrated that hsa-miR-1269a overexpression downregulated FAM46C. Rescue experiments revealed that hsa-miR-1269a accelerated the malignant progression of ESCC through FAM46C down-regulation. These results indicate that the interaction between hsa-miR-1269a and FAM46C plays a regulatory role in driving the malignant progression of ESCC cells, thereby providing a novel molecular mechanism for understanding ESCC.
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