Abstract
ErbB4 is an important member of ErbB subfamily of tyrosine kinases receptor with overexpression in several tumors; however its biological role in esophageal cancer is poorly understood till date. The main objective of this study was to examine whether miRNA-140-5p could target and control ErbB4 expression at transcriptional level. The ErbB4 expressions in different cell lines were evaluated by western blotting and luciferase assay. Moreover, cell proliferation, apoptosis, and cell invasion studies were investigated using MTT, flow cytometry, and transwell assays. miRNA-140-5p remarkably downregulated the ErbB4 expression in EC9706 and TE-1A cell lines. Furthermore, miRNA-140-5p transfected cell significantly controlled the cell proliferation and enhanced the apoptosis of multiple cells. Additionally, miRNA-140-5p had marked effect on the DNA synthesis and caspase 3/7 activity in comparison to control cells. Specifically, miRNA-140-5p inhibited/repressed the cancer cell invasion and migration in a sign to have important biological role in esophageal carcinomas. Taken together, miRNA-140-5p could act as a potential molecular target in ErbB4 overexpressing ESCC cell lines paving the way for effective esophageal cancer treatment.
Highlights
Esophageal cancer is one of the most fatal cancers worldwide with high prevalence in East Asian countries (China) [1]
First we examined the ErbB4 protein expression in 4 different esophageal normal (HET-1A) and cancer cell lines (Eca109, Ec9706, and TE-1). It is evident from western blot analysis that all the esophageal cancer cell lines have expressed significantly higher levels of ErbB4 protein, while, on the other hand, HET-1A showed the lowest expression levels for ErbB4
Having confirmed ErbB4 as the functional target for miR-140-5p, we examined whether the miRNA can be effective to control or limit the cell proliferation activity in esophageal cancer cell lines such as EC-9706 and TE-1A cells
Summary
Esophageal cancer is one of the most fatal cancers worldwide with high prevalence in East Asian countries (China) [1]. Present treatment strategies include chemotherapy, radiation therapy, and surgical removal of tumors; none can improve the tumor progression profile in esophageal cancer [4, 5]. In this regard, molecularly targeted therapies attracted significant attention of researchers in the recent past [6]. ErbB1 and ErbB2 are one of the well-known oncogenes and many therapeutic moieties have been approved targeting these receptors. These tyrosine kinase receptors have been reportedly overexpressed in many cancerous tissues and considered as one of the important clinical markers [10, 11]. The signaling pathways include mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3-K)/Akt pathways [19, 20]
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