Abstract
BackgroundMicroRNA-106b (miR-106b) was recently identified as an oncogene participating in cancer progression. Transforming growth factor β1(TGF-β1) is an indispensable cytokine regulating the local microenvironment, thereby promoting cervical cancer progression. However, the roles of miR-106b in cervical carcinoma progression and TGF-β1-involvement in the tumorigenesis of cervical cancer remain unknown.MethodsThe expression of miR-106b in human cervical specimens was detected by real-time PCR analysis and in situ hybridization assay. The effect of miR-106b on cell migration was analyzed by scratch and transwell assays. TGF-β1 was used to induce cell migration. The expression of the miR-106b target gene DAB2 in human cervical tissues and cell lines were measured by qRT-PCR, western blot and immunohistochemistry. Dual-luciferase reporter assay was used to identify DAB2 as a miR-106b-directed target gene.ResultsmiR-106b was frequently up-regulated in human cervical carcinoma specimens and cervical cancer cell lines. Over-expression of miR-106b significantly promoted HeLa and SiHa cells migration. Likewise, inhibition of miR-106b decreased HeLa and SiHa cells migration. The multifunctional cytokine TGF-β facilitates metastasis in cervical carcinoma. miR-106b inhibitor treatment decreased the TGF-β1-stimulated migration of HeLa and SiHa cells. DAB2, a predicted target gene of miR-106b, was inhibited by TGF-β1 partly through miR-106b and was involved in TGF-β1-induced cervical cancer cell migration. The expression of DAB2 was low in cervical cancer tissues, and negatively correlated with miR-106b expression. Finally, DAB2 was identified as a miR-106b-directed target gene by dual-luciferase reporter assay.ConclusionOur data suggest that the TGF-β1/miR-106b/DAB2 axis may be involved in the pathogenesis of cervical carcinoma.
Highlights
MicroRNA-106b was recently identified as an oncogene participating in cancer progression
The high expression of miR106b was associated with lymph node metastasis in breast cancer. miR-106b promotes the activation of Wnt signal and induces β-catenin to enter the nucleus, thereby enhancing the ability of tumor cell invasion and migration [12]. miR-106b has been shown to participate in activation of the transforming growth factor-β (TGF-β)/Smad signaling pathway by inhibiting Smad7 protein expression to intensify the epithelial mesenchymal transition (EMT) in breast cancer cells [13]
We found that miR-106b had high expression in cervical cancer and promoted the migration of cervical cancer cells. miR-106b was involved in TGF-β1-induced cell migration by targeting disabled homolog 2 (DAB2) in cervical carcinoma
Summary
MicroRNA-106b (miR-106b) was recently identified as an oncogene participating in cancer progression. Transforming growth factor β1(TGF-β1) is an indispensable cytokine regulating the local microenvironment, thereby promoting cervical cancer progression. Parametrical infiltration and distant metastasis of refractory cervical miRNAs are single-stranded RNAs of about 21–23 nt that play roles in posttranscriptional regulation of target genes in cancer development, cell proliferation, apoptosis and differentiation [6,7,8,9]. MiR-106b promotes the activation of Wnt signal and induces β-catenin to enter the nucleus, thereby enhancing the ability of tumor cell invasion and migration [12]. MiR-106b has been shown to participate in activation of the TGF-β/Smad signaling pathway by inhibiting Smad protein expression to intensify the epithelial mesenchymal transition (EMT) in breast cancer cells [13] The high expression of miR106b was associated with lymph node metastasis in breast cancer. miR-106b promotes the activation of Wnt signal and induces β-catenin to enter the nucleus, thereby enhancing the ability of tumor cell invasion and migration [12]. miR-106b has been shown to participate in activation of the TGF-β/Smad signaling pathway by inhibiting Smad protein expression to intensify the epithelial mesenchymal transition (EMT) in breast cancer cells [13]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callMore From: Journal of Experimental & Clinical Cancer Research
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
