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Cancer Med. 2017 Dec;6(12):2957-2965. doi: 10.1002/cam4.1214. Epub 2017 Oct 16.

miR-1 suppresses the proliferation and promotes the apoptosis of esophageal carcinoma cells by targeting Src.

Author information

1
Department of Thoracic and Cardiovascular Surgery, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu, 210008, China.
2
Nanjing Medical University Affiliated Cancer Hospital, Nanjing, Jiangsu, 210009, China.
3
State Key Laboratory of Pharmaceutical Biotechnology, Nanjing Advanced Institute of Life Sciences, Jiangsu Engineering Research Center for MicroRNA Biology and Biotechnology, Nanjing, Jiangsu, 210093, China.
4
Department of Lymphoma, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center of Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, 300060, China.
5
Nanjing Multicenter Biobank, Biobank of Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu, 210008, China.

Abstract

Nonreceptor tyrosine kinase c-Src, also known as Src, is a potent oncogene involved in a series of biological processes including cell growth, differentiation, and apoptosis; however, its expression pattern and function in esophageal cancer is poorly addressed. In this study, abnormal overexpression of Src protein was observed in esophageal cancer tissues, which fuelled the speculation that microRNA-mediated posttranscriptional regulatory mechanism might be involved. Bioinformatic analyses were applied to identify miRNAs that could potentially target Src. miR-1 was predicted and further validated as a direct repressor of Src. Moreover, we manipulated knockdown and overexpression experiment on TE-1 and TE-10 cells to demonstrate miR-1 suppressed proliferation and promoted apoptosis in esophageal cancer cells by inhibiting Src. Taken together, this study underlines a negative regulatory mechanism in which miR-1 serves as a suppressor of Src in esophageal cancer cells and may provide insights into novel therapeutic approaches for esophageal cancer.

KEYWORDS:

Src; apoptosis; esophageal cancer; miR-1; proliferation

PMID:
29034995
PMCID:
PMC5727306
DOI:
10.1002/cam4.1214
[Indexed for MEDLINE]
Free PMC Article

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