TY - JOUR
T1 - miR-93-5p regulates the occurrence and development of esophageal carcinoma epithelial cells by targeting TGFβR2
AU - CAI, YIBIN
AU - RUAN, WEIZHONG
AU - DING, JIANMING
AU - WEI, NING
AU - WANG, JIANCHAO
AU - ZHANG, HONG
AU - MA, NING
AU - WENG, GUIBIN
AU - SU, WEI KUN
AU - LIN, YIJIN
AU - ZHU, KUNSHOU
N1 - Publisher Copyright:
© 2021 Spandidos Publications. All rights reserved.
PY - 2021/3
Y1 - 2021/3
N2 - Emerging studies have indicated that the dysregulation of microRNAs (miRNAs or miRs) plays a vital role in the development and metastasis of tumors. However, the role of miR-93-5p in esophageal carcinoma (EC) has not been extensively reported. The present study thus focused on the role of miR-93-5p and its downstream target in the occurrence and development of EC. Firstly, miRNA expression profiles associated with EC were accessed from the TCGA-ESCA dataset and analyzed. Subsequently, the expression patterns of miR-93-5p and TGFβR2 were characterized in the human esophageal cell line, Het-1A, and the human EC cell lines, TE-1, Eca-109 and EC9706, by RT-qPCR and western blot analysis. WST-1 assay, flow cytometry, Transwell assay, wound healing assay and bioinformatics analysis were used to explore their functions in EC cells. Finally, a dual-luciferase reporter assay was employed to determine the targeted association between miR-93-5p and TGFβR2. The results revealed that the expression of miR-93-5p was markedly higher in EC cell lines compared with that in the normal cell line. The overexpression of miR-93-5p facilitated cell proliferation, migration and invasion, and inhibited cell apoptosis. Additionally, TGFβR2 was identified as a functional target of miR-93-5p in EC cells, as judged by a series of in vitro experiments. Furthermore, it was found that the simultaneous overexpression of miR-93-5p and TGFβR2 almost had no effect on the biological behaviors of EC cells. On the whole, the present study demonstrates that miR-93-5p promotes the proliferation, migration and invasion, and inhibits the apoptosis of EC cells by targeting TGFβR2.
AB - Emerging studies have indicated that the dysregulation of microRNAs (miRNAs or miRs) plays a vital role in the development and metastasis of tumors. However, the role of miR-93-5p in esophageal carcinoma (EC) has not been extensively reported. The present study thus focused on the role of miR-93-5p and its downstream target in the occurrence and development of EC. Firstly, miRNA expression profiles associated with EC were accessed from the TCGA-ESCA dataset and analyzed. Subsequently, the expression patterns of miR-93-5p and TGFβR2 were characterized in the human esophageal cell line, Het-1A, and the human EC cell lines, TE-1, Eca-109 and EC9706, by RT-qPCR and western blot analysis. WST-1 assay, flow cytometry, Transwell assay, wound healing assay and bioinformatics analysis were used to explore their functions in EC cells. Finally, a dual-luciferase reporter assay was employed to determine the targeted association between miR-93-5p and TGFβR2. The results revealed that the expression of miR-93-5p was markedly higher in EC cell lines compared with that in the normal cell line. The overexpression of miR-93-5p facilitated cell proliferation, migration and invasion, and inhibited cell apoptosis. Additionally, TGFβR2 was identified as a functional target of miR-93-5p in EC cells, as judged by a series of in vitro experiments. Furthermore, it was found that the simultaneous overexpression of miR-93-5p and TGFβR2 almost had no effect on the biological behaviors of EC cells. On the whole, the present study demonstrates that miR-93-5p promotes the proliferation, migration and invasion, and inhibits the apoptosis of EC cells by targeting TGFβR2.
KW - Apoptosis
KW - Esophageal carcinoma
KW - MiR-93-5p
KW - Migration and invasion
KW - Proliferation
KW - Transforming growth factor-β receptor 2
UR - http://www.scopus.com/inward/record.url?scp=85099302485&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85099302485&partnerID=8YFLogxK
U2 - 10.3892/ijmm.2020.4836
DO - 10.3892/ijmm.2020.4836
M3 - Article
C2 - 33448310
AN - SCOPUS:85099302485
SN - 1107-3756
VL - 47
JO - International journal of molecular medicine
JF - International journal of molecular medicine
IS - 3
M1 - 4836
ER -