Alternative titles; symbols
HGNC Approved Gene Symbol: MIR106B
Cytogenetic location: 7q22.1 Genomic coordinates (GRCh38): 7:100,093,993-100,094,074 (from NCBI)
MicroRNAs (miRNAs), like MIR106B, are short noncoding RNAs that regulate gene expression by binding complementary sequences in the 3-prime UTRs of target mRNAs and either inhibiting their translation or inducing their degradation (Petrocca et al., 2008).
By sequence analysis, Ivanovska et al. (2008) identified 18 miRNAs as members of the MIR106B family of miRNAs. The seed sequences of several of these miRNAs, including MIR106A (300792), are identical to that of MIR106B.
Petrocca et al. (2008) found that MCM7 (600592) and the precursors of miRNAs MIR106B, MIR93 (612984), and MIR25 (612150), all of which arise from intron 13 of the MCM7 gene, were overexpressed with almost perfect correlation in 5 of 10 human gastric tumors. Accumulation of precursor RNA containing MCM7, MIR106B, MIR93, and MIR25 was induced following entry into G1 phase in a synchronized human gastric cancer cell line and was associated with expression of the master cell cycle regulator E2F1 (189971). The 3-prime UTR of the E2F1 transcript contains MIR106B- and MIR93-binding sites, suggesting that E2F1 is regulated by these miRNAs in a negative-feedback loop. Overexpression, knockdown, and mutation studies confirmed that E2F1 is a target for MIR106B and MIR93. In addition, overexpression of MIR106B, MIR93, and MIR25 in gastric cancer cells reduced cell response to TGF-beta (TGFB1; 190180) by interfering with synthesis of p21 (CDKN1A; 116899) and BIM (BCL2L11; 603827), the 2 most downstream effectors of TGF-beta-dependent cell cycle arrest and apoptosis, respectively. Petrocca et al. (2008) concluded that the MIR106B-MIR93-MIR25 cluster, which is activated by E2F1 and upregulated in human adenocarcinomas, alters the response of gastric cancer cells to TGF-beta, affecting both cell cycle arrest and apoptosis.
Ivanovska et al. (2008) found that expression of several members of the MIR106B family, including MIR106B, was upregulated in several human tumors compared with adjacent normal tissues. Microarray analysis showed that expression of MIR106B and MIR106A correlated with expression of genes involved in DNA replication and mitosis, while expression of MIR93, another MIR106B family member, correlated with expression of genes involved in DNA replication only. Transfection of human cells with synthetic RNA duplexes to mimic miRNAs showed that MIR106B and MIR106A, but not MIR93, increased the number of cells in S phase. Cell cycle inhibitor studies showed that MIR106B and MIR106A mimics functioned as positive regulators of the G1-to-S transition, and mutation of nucleotides 2 and 3 of MIR106B abrogated the effect. Microarray analysis revealed that these miRNAs targeted cell cycle regulators, and silencing of p21 alone, which contains 2 MIR106B-binding hexamers in its 3-prime UTR, fully reflected the phenotype. MIR106B overexpression overrode DNA damage-induced checkpoint established by TP53 (191170)-p21 pathway.
Petrocca et al. (2008) reported that the MIR106B, MIR93, and MIR25 genes map to chromosome 7q22 and are clustered in a 5-prime to 3-prime orientation within intron 13 of the MCM7 gene.
Fontana et al. (2007) stated that the miRNA gene cluster on chromosome 7 that contains MIR106B and MIR25 is highly homologous to a cluster on chromosome 13 that contains MIR17 (609416), MIR18A (609417), and MIR92A1 (609422), and another on chromosome X that contains MIR106A (300792) and MIR92A2 (301092).
Fontana, L., Pelosi, E., Greco, P., Racanicchi, S., Testa, U., Liuzzi, F., Croce, C. M., Brunetti, E., Grignani, F., Peschle, C. MicroRNAs 17-5p-20a-106a control monocytopoiesis through AML1 targeting and M-CSF receptor upregulation. Nature Cell Biol. 9: 775-787, 2007. [PubMed: 17589498] [Full Text: https://doi.org/10.1038/ncb1613]
Ivanovska, I., Ball, A. S., Diaz, R. L., Magnus, J. F., Kibukawa, M., Schelter, J. M., Kobayashi, S. V., Lim, L., Burchard, J., Jackson, A. L., Linsley, P. S., Cleary, M. A. MicroRNAs in the miR-106b family regulate p21/CDKN1A and promote cell cycle progression. Molec. Cell. Biol. 28: 2167-2174, 2008. [PubMed: 18212054] [Full Text: https://doi.org/10.1128/MCB.01977-07]
Petrocca, F., Visone, R., Onelli, M. R., Shah, M. H., Nicoloso, M. S., de Martino, I., Iliopoulos, D., Pilozzi, E., Liu, C.-G., Negrini, M., Cavazzini, L., Volinia, S., Alder, H., Ruco, L. P., Baldassarre, G., Croce, C. M., Vecchione, A. E2F1-regulated microRNAs impair TGF-beta-dependent cell-cycle arrest and apoptosis in gastric cancer. Cancer Cell 13: 272-286, 2008. [PubMed: 18328430] [Full Text: https://doi.org/10.1016/j.ccr.2008.02.013]