INTRODUCTIONOrofacial clefts are major craniofacial congenital abnormalities, characterized by unsuccessful fusion of normal facial processes (Fraser, ; Mossey, Little, Munger, Dixon, & Shaw, ). Non‐syndromic orofacial clefts (NSOC), without any other major developmental accompanied abnormalities, constituted the majority of orofacial clefts (Cobourne, ). Among all the risk factors during NSOC progression, the genetic factor takes a critical role. There are three main types of orofacial clefts: cleft lip only (CLO), cleft lip with palate (CLP), and cleft palate only (CPO) (Lacheretz & Poupard, ). Depending on the similarities in both epidemiologic features and embryologic timing, CLP and CLO are traditionally grouped together to form the group cleft lip with or without cleft palate (CL/P) (Lidral, Moreno, & Bullard, ).MicroRNAs (miRNAs) are endogenous non‐coding RNAs participating in the regulation of process of life, such as proliferation and apoptosis, among other biological processes (Bentwich et al., ). MiRNAs played important roles in craniofacial development. For instance, a recent study showed that miRNA‐23b and miRNA‐133b participated in mid‐facial developmental process (Ding et al., ).Expression and synthesis of miRNAs are regulated by miRNA processing genes. Initially, primary miRNAs (pri‐miRNAs) are transcribed by RNA polymeraseII inside nucleus. DROSHA (RNAseIII) and its cofactor DGCR8 cleave pri‐miRNAs, and
Oral Diseases – Wiley
Published: Jan 1, 2018
Keywords: ; ; ;
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