MiR-106b promotes migration and invasion through enhancing EMT via downregulation of Smad 7 in Kazakh’s esophageal squamous cell carcinoma
- 12 September 2016
- journal article
- research article
- Published by Springer Science and Business Media LLC in Tumor Biology
- Vol. 37 (11), 14595-14604
- https://doi.org/10.1007/s13277-016-5338-x
Abstract
Accumulated evidence suggests that miR-106b played a key role in the promotion of the metastases of cancer; however, little is known about miR-106b in esophageal squamous cell carcinoma (ESCC). To investigate expression level of miR-106b in ESCC tissues, quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect miR-106b expression in 35 Kazakh’s ESCC and paired normal adjacent tissues (NATs). To evaluate the role mediated by miR-106b in the proliferation, migration, and invasion, MTT, wound healing, and transwell assays were employed, respectively. Luciferase reporter assay was used to identify the downstream target through miR-106b. To understand the regulation between miR-106b and Smad 7, qRT-PCR and western blot were performed. The present study showed that miR-106b was pronouncedly upregulated in ESCC relative to paired NAT and that upregulated miR-106b was significantly associated with lymph node metastases. MiR-106b was found to be able to promote proliferation, migration, and invasion of ESCC cells in vitro. Smad 7 was confirmed as a downstream target of miR-106b in our experimental setting. Smad 7 was remarkably downregulated in ESCC compared with paired NAT. In addition, upregulation of miR-106b can promote epithelial mesenchymal transition (EMT) in ESCC cell in vitro. Our results indicated that miR-106b can promote migration and invasion of ESCC cells through enhancing EMT process via downregulation of Smad 7, suggesting that miR-106b can be a potential molecular phenotype in ESCC metastases.Keywords
Funding Information
- National Natural Science Foundation of China (No.81160303, 81260359, U1303321)
This publication has 33 references indexed in Scilit:
- Low adherent cancer cell subpopulations are enriched in tumorigenic and metastatic epithelial-to-mesenchymal transition-induced cancer stem-like cellsScientific Reports, 2016
- miR-93 promotes TGF-β-induced epithelial-to-mesenchymal transition through downregulation of NEDD4L in lung cancer cellsTumor Biology, 2015
- miR-106b-5p targets tumor suppressor gene SETD2 to inactive its function in clear cell renal cell carcinomaOncotarget, 2015
- Esophageal cancer: Risk factors, screening and endoscopic treatment in Western and Eastern countriesWorld Journal of Gastroenterology, 2015
- Lymph Node Metastases in Esophageal Carcinoma: An Endoscopist's ViewClinical Endoscopy, 2014
- MicroRNA‐106b regulates the tumor suppressor RUNX3 in laryngeal carcinoma cellsFEBS Letters, 2013
- MicorRNA 106b ∼ 25 cluster and gastric cancerSurgical Oncology, 2013
- Causes and Consequences of MicroRNA DysregulationThe Cancer Journal, 2012
- Comprehensive MicroRNA Profiling for Head and Neck Squamous Cell CarcinomasClinical Cancer Research, 2010
- Role of the miR‐106b‐25 microRNA cluster in hepatocellular carcinomaCancer Science, 2009