MicroRNA-27 promotes the differentiation of odontoblastic cell by targeting APC and activating Wnt/β-catenin signaling.
MicroRNAs (miRNAs) play an essential role in regulating cell differentiation either by inhibiting mRNA translation or by inducing its degradation. However, the role of miRNAs in odontoblastic cell differentaion is largely unknown. In the present study, we demonstrate that the expression of miR-27 was significantly increased during MDPC-23 odontoblastic cell differentiation. Furthermore, the up-regulation of miR-27 promotes the differentiation of MDPC-23 odontoblastic cells and accelerates mineralization without cell proliferation. In addition, our results of target gene prediction revealed that the mRNA of adenomatous polyposis coli (APC) associated with Wnt/β-catenin signaling pathway has miR-27 binding site in the its 3' UTR and is suppressed by miR-27. Subsequentially, the down-regulated APC by miR-27 triggered the activation of Wnt/β-catenin signaling through accumulation of β-catenin in the nucleus. Our data suggest that miR-27 promotes MDPC-23 odontoblastic cell differentiation by targeting APC and activating Wnt/β-catenin signaling. Therefore, miR-27 might be considered a critical candidate as an odontoblastic differentiation molecular target for the development of miRNA based therapeutic agents in the dental medicine.
Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju 501-759, Republic of Korea.
Min-Gyeong
MG
Park
Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju 501-759, Republic of Korea.
Jae-Sung
JS
Kim
Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju 501-759, Republic of Korea.
Sun-Young
SY
Park
Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju 501-759, Republic of Korea.
Seul Ah
SA
Lee
Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju 501-759, Republic of Korea.
Heung-Joong
HJ
Kim
Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju 501-759, Republic of Korea.
Chun Sung
CS
Kim
Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju 501-759, Republic of Korea.
Jin-Soo
JS
Kim
Department of Biotechnology, Chosun University, Gwangju 501-759, Republic of Korea.
Hong Sung
HS
Chun
Department of Oral Histology-Developmental Biology, School of Dentistry and Dental Research Institute, BK 21, Seoul National University, Seoul 110-749, Republic of Korea.
Joo-Cheol
JC
Park
Oral Biology Research Institute, Chosun University School of Dentistry, Gwangju 501-759, Republic of Korea. Electronic address: kdk@chosun.ac.kr.
Do Kyung
DK
Kim
D025601:Adenomatous Polyposis Coli Protein / Q000235:genetics*; D000818:Animals; D002454:Cell Differentiation / Q000235:genetics / Q000502:physiology; D002460:Cell Line; D015870:Gene Expression; D051379:Mice; D035683:MicroRNAs / Q000235:genetics* / Q000378:metabolism*; D009804:Odontoblasts / Q000166:cytology* / Q000378:metabolism*; D009805:Odontogenesis / Q000235:genetics / Q000502:physiology; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D014074:Tooth Calcification / Q000235:genetics / Q000502:physiology; D060449:Wnt Signaling Pathway; D051176:beta Catenin / Q000378:metabolism*
D025601:Adenomatous Polyposis Coli Protein; C495267:CTNNB1 protein, mouse; D035683:MicroRNAs; C540674:Mirn27 microRNA, mouse; D012333:RNA, Messenger; D051176:beta Catenin
Adenomatous polyposis coli; Differentiation; Odontoblasts; miR-27; β-Catenin