MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

Li, Xia; Zhou, Qi; Tao, Ling; Yu, Chunxia

doi:10.3892/or.2017.5832

Cited by 23 publications

(21 citation statements)

References 33 publications

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“…The oncogenic role of hsa-mir-106a-363 cluster has been much less extensively studied, specifically in the context of leukemia. There are few reports indicating an oncogenic potential of miRNAs from this cluster in human malignancies [93], [94], [95]. Interestingly, Dylla and Jedlicka demonstrated the importance of the cooperative oncogenic activity of miRNAs from this cluster in Ewing sarcoma cell lines; blockade of individual miRNAs had little or no inhibitory effect on growth of the cells in contrast to the blockade of the whole cluster [94].…”

Section: Discussionmentioning

confidence: 99%

Comprehensive Investigation of miRNome Identifies Novel Candidate miRNA-mRNA Interactions Implicated in T-Cell Acute Lymphoblastic Leukemia

et al. 2019

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T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy originating from T-cell precursors. The genetic landscape of T-ALL has been largely characterized by next-generation sequencing. Yet, the transcriptome of miRNAs (miRNome) of T-ALL has been less extensively studied. Using small RNA sequencing, we characterized the miRNome of 34 pediatric T-ALL samples, including the expression of isomiRs and the identification of candidate novel miRNAs (not previously annotated in miRBase). For the first time, we show that immunophenotypic subtypes of T-ALL present different miRNA expression profiles. To extend miRNome characteristics in T-ALL (to 82 T-ALL cases), we combined our small RNA-seq results with data available in Gene Expression Omnibus. We report on miRNAs most abundantly expressed in pediatric T-ALL and miRNAs differentially expressed in T-ALL versus normal mature T-lymphocytes and thymocytes, representing candidate oncogenic and tumor suppressor miRNAs. Using eight target prediction algorithms and pathway enrichment analysis, we identified differentially expressed miRNAs and their predicted targets implicated in processes (defined in Gene Ontology and Kyoto Encyclopedia of Genes and Genomes) of potential importance in pathogenesis of T-ALL, including interleukin-6–mediated signaling, mTOR signaling, and regulation of apoptosis. We finally focused on hsa-mir-106a-363 cluster and functionally validated direct interactions of hsa-miR-20b-5p and hsa-miR-363-3p with 3′ untranslated regions of their predicted targets ( PTEN , SOS1 , LATS2 ), overrepresented in regulation of apoptosis. hsa-mir-106a-363 is a paralogue of prototypic oncogenic hsa-mir-17-92 cluster with yet unestablished role in the pathogenesis of T-ALL. Our study provides a firm basis and data resource for functional analyses on the role of miRNA-mRNA interactions in T-ALL.

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Section: Discussionmentioning

confidence: 99%

Comprehensive Investigation of miRNome Identifies Novel Candidate miRNA-mRNA Interactions Implicated in T-Cell Acute Lymphoblastic Leukemia

et al. 2019

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“…Increasing evidence has indicated that the enhanced motility and invasiveness of cancer cells are associated with the progression of cervical cancer (14-16). In the present study, we observed that overexpression of S100A9 promoted the proliferation and migration of cervical cancer cells, eventually facilitating EMT, which was regulated by the Wnt/β-catenin signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

S100A9 promotes the proliferation and migration of cervical cancer cells by inducing epithelial‑mesenchymal transition and activating the Wnt/β‑catenin pathway

Zha

Sun

et al. 2019

Int J Oncol

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S100 calcium-binding protein A9 (S100A9), a member of the S100 protein family, is often upregulated in various cancers, including cervical cancer. Elevated S100A9 expression is thought to serve an important role in tumorigenesis; however, the exact role of S100A9 in the modulation of cervical cancer and the underlying molecular mechanism remain unknown. In the present study, we aimed to investigate the effects of S100A9 on the proliferation and migration of cervical cancer cells, as well as the molecular mechanisms underlying these effects. Our results demonstrated that endogenous expression of S100A9 in SiHa and CaSki cell lines was significantly higher than in the HeLa cell line. As expected, overexpression of S100A9 enhanced the proliferation and migration of cervical cancer cells. In addition, S100A9 overexpression induced epithelial-mesenchymal transition (EMT) as determined by reduced expression levels of the epithelial marker E-cadherin, whereas the expression levels of the mesenchymal marker vimentin were upregulated. Furthermore, it was reported that the effects of S100A9 in the modulation of cervical cancer cells were mediated through the Wnt/β-catenin signaling pathway as β-catenin knockdown significantly suppressed the ability of S100A9 to enhance the proliferation and migration of cervical cancer cells. Collectively, these findings suggest that S100A9 promoted the proliferation and migration of cervical cancer cell lines. Furthermore, the underlying molecular mechanisms may be partially attributed to the induction of EMT and activation of the Wnt/β-catenin signaling pathway.

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“…Metastasis-associated protein 1 (MTA-1), matrix metalloproteinase (MMP)2, and MMP9 are important components of the matrix metalloproteinase family, which can hydrolyze intercellular matrix proteins, providing cells with the ability to metastasize [31]. Tissue inhibitor of metalloproteinases 2 (TIMP2) can inhibit MMPs, while increased expression of E-cadherin, vimentin, and collagen I protein stabilize cells [32]. The migration and invasive ability of malignant cells have previously been shown to be associated with overexpression of MTA-1, MMP2, and MMP9 and inhibition of TIMP-2 expression [30–32].…”

Section: Discussionmentioning

confidence: 99%

“…Tissue inhibitor of metalloproteinases 2 (TIMP2) can inhibit MMPs, while increased expression of E-cadherin, vimentin, and collagen I protein stabilize cells [32]. The migration and invasive ability of malignant cells have previously been shown to be associated with overexpression of MTA-1, MMP2, and MMP9 and inhibition of TIMP-2 expression [30–32]. The results of this study showed that after silencing of the MYH10 gene, the expression levels of MTA-1, MMP2, and MMP9 genes and proteins were significantly down-regulated, whereas TIMP-2 was upregulated.…”

Section: Discussionmentioning

confidence: 99%

Myosin Heavy Chain 10 (MYH10) Gene Silencing Reduces Cell Migration and Invasion in the Glioma Cell Lines U251, T98G, and SHG44 by Inhibiting the Wnt/β-Catenin Pathway

et al. 2018

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BackgroundThe myosin heavy chain 10 or MYH10 gene encodes non-muscle myosin II B (NM IIB), and is involved in tumor cell migration, invasion, extracellular matrix (ECM) production, and epithelial-mesenchymal transition (EMT). This study aimed to investigate the effects of the MYH10 gene on normal human glial cells and glioma cell lines in vitro, by gene silencing, and to determine the signaling pathways involved.Material/MethodsThe normal human glial cell line HEB, and the glioma cell lines, U251, T98G, and SHG44 were studied. Plasmid transfection silenced the MYH10 gene. The cell counting kit-8 (CCK-8) assay evaluated cell viability. Cell migration and invasion were evaluated using scratch and transwell assays. Western blot measured the protein expression levels, and quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the mRNA expression levels, for MYH10, metastasis-associated protein 1 (MTA-1), matrix metalloproteinase (MMP)-1, MMP-9, tissue inhibitor of metalloproteinases 2 (TIMP2), collagen 1, E-cadherin, vimentin, Wnt3a, β-catenin, and cyclin D1.ResultsThe MYH10 gene was overexpressed in U251, T98G, and SHG44 cells. MYH10 expression was down-regulated following siMYH10 plasmid interference, which also inhibited glioma cell migration and invasion. MYH10 gene silencing resulted in reduced expression of MTA-1, MPP-2, MMP-9 and vimentin, and increased expression of TIMP-2, E-cadherin and collagen 1 at the protein and mRNA level, and inhibited the Wnt/β-catenin pathway.ConclusionsIn human glioma cell lines, silencing the MYH10 gene reduced cell migration and invasion, by inhibiting the Wnt/β-catenin pathway, which may regulate the ECM and inhibit EMT in human glioma.

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MicroRNA-106a promotes cell migration and invasion by targeting tissue inhibitor of matrix metalloproteinase 2 in cervical cancer

Cited by 23 publications

References 33 publications

Comprehensive Investigation of miRNome Identifies Novel Candidate miRNA-mRNA Interactions Implicated in T-Cell Acute Lymphoblastic Leukemia

Comprehensive Investigation of miRNome Identifies Novel Candidate miRNA-mRNA Interactions Implicated in T-Cell Acute Lymphoblastic Leukemia

S100A9 promotes the proliferation and migration of cervical cancer cells by inducing epithelial‑mesenchymal transition and activating the Wnt/β‑catenin pathway

Myosin Heavy Chain 10 (MYH10) Gene Silencing Reduces Cell Migration and Invasion in the Glioma Cell Lines U251, T98G, and SHG44 by Inhibiting the Wnt/β-Catenin Pathway

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