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
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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页数:9
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