Abstract
MicroRNA (miR)-106b serves an essential function in a variety of human cancer types, particularly in the process of invasion and metastasis. However, the function and mechanism of miR-106b in the invasion and metastasis of esophageal squamous cell carcinoma (ESCC) has remained elusive. In the present study, it was demonstrated that miR-106b was upregulated in ESCC tissues and cell lines. Furthermore, miR-106b expression in ESCC tissues was positively associated with lymphatic metastasis. Inhibition of miR-106b in EC-1 and EC9706 cells decreased not only the invasion and metastasis ability but also the proliferation ability of EC-1 and EC9706 cells. In addition, miR-106b had the ability to induce epithelial-to-mesenchymal transition (EMT) in EC-1 and EC9706 cells. In terms of the underlying mechanism, it was revealed that miR-106b promoted the invasion, metastasis and proliferation ability of EC-1 and EC9706 cells by directly targeting phosphatase and tension homolog (PTEN). Furthermore, miR-106b induced EMT in EC-1 and EC9706 cells by suppressing the expression of PTEN. In summary, the present study revealed that miR-106b contributed to invasion and metastasis in ESCC by regulating PTEN mediated EMT. Downregulation of miR-106b may be a novel strategy for preventing tumor invasion and metastasis.
Highlights
Esophageal squamous cell carcinoma (ESCC) is the most malignant lesion in China, in Linzhou, Henan [1].Key words: esophageal squamous cell carcinoma, microRNA‐106b, invasion and metastasis, phosphatase and tensin homolog, epithelial‐to‐mesenchymal transitionTreatment of ESCC is largely useless due to the occurrence of invasion and metastasis in the early stage
Results miR‐106b was upregulated in ESCC tissues and cell lines
The results revealed that the expression levels of miR‐106b in ESCC tissues were significantly increased compared with those in adjacent normal mucosa tissue (P
Summary
Esophageal squamous cell carcinoma (ESCC) is the most malignant lesion in China, in Linzhou, Henan [1]. MiRNAs have been demonstrated to serve notable functions in tumor invasion and metastasis by functioning as EMT suppressors or inducers [5,6]. Whether miR‐106b participates in the invasion and metastasis process of ESCC by inducing EMT and the mechanism of how miR‐106b induces EMT in ESCC had not been fully explored until now. MiRNAs participate in the occurrence and development of a cancer by regulating the post‐transcriptional process of their target gene. One previous study had reported that PTEN served as a tumor‐suppressing gene in cancer invasion and metastasis [14]. Whether miR‐106b regulates the expression and activity of PTEN in ESCC has never been previously elucidated, to the best of our knowledge. MiR‐106b may participate in the invasion and metastasis of ESCC via PTEN mediated EMT
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