MicroRNA-10b mediates TGF-β1-regulated glioblastoma proliferation, migration and epithelial-mesenchymal transition

Ma, Chao; Feng, Wei; Xia, Huan; Liu, Haiyu; Xin, Dong; Zhang, Yandong; Luo, Qiong; Liu, Yan; Li, Yang

doi:10.3892/ijo.2017.3947

Cited by 43 publications

(38 citation statements)

References 46 publications

(50 reference statements)

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“…In tumors, TGF-β, once activated, promotes cell growth, migration and invasion (29,30), therefore, the level of TGF-β expression in tumors is also related to the degree of malignancy of the tumor. A previous study demonstrated that TGF-β promotes the migration of human glioma cells by promoting the expression of miR-10b (31). In the present study, it was demonstrated that the proliferation of esophageal cancer cells increased along with an increase of TGF-β concentration.…”

Section: Discussionsupporting

confidence: 65%

Effect and mechanism of microRNA‑10b on proliferation and invasion of esophageal cancer cells

Liu

Salai

et al. 2019

Exp Ther Med

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MicroRNA (miR)-10b is highly expressed in esophageal cancer tissues and is associated with poor prognosis of esophageal cancer. However, the role and mechanism of miR-10b in esophageal cancer cells remains unclear, therefore, the present study aimed to investigate this. Esophageal cancer cells, TE-1 and EC9706, were transfected with miR-10b mimic, miR-10b inhibitor or incubated with transforming growth factor-β (TGF-β). MTT and EdU assays were used to detect cell proliferation. Flow cytometry was used to determine cell cycle analysis and apoptosis. Cell migration and invasion were also analyzed. Western blot analysis was used to detect protein levels and reverse transcription-quantitative PCR was used to analyze miR-10b expression. The present results demonstrated that, compared with the control group, miR-10b significantly promoted TE-1 and EC9706 cell proliferation. Compared with miR-10b inhibitor group and control group, miR-10b mimic promoted esophageal cancer cell cycle progression, inhibited apoptosis of esophageal cancer cells and promoted the migration and invasion of cells. The proliferation of esophageal cancer cells increased in a dose-dependent manner with TGF-β concentration. TGF-β treatment induced high expression of miR-10b in both cell lines. The miR-10b mimic + TGF-β group further promoted the migration and invasion of esophageal cancer cells. Western blot analysis determined that, compared with the control group, miR-10b mimic increased TGF-β expression. miR-10b mimic also inhibited the expression of phosphatase and tensin homolog (PTEN) in tumor cells. Compared with the control group, TGF-β inhibited the expression of PTEN with the miR-10b mimic + TGF-β group further inhibiting the PTEN. miR-10b inhibitor + TGF-β reversed the effect of TGF-β and miR-10b on PTEN. In conclusion, miR-10b promoted cell cycle progression, inhibited apoptosis and promoted the migration and invasion of esophageal cancer cells. The mechanism may be related to the upregulation of TGF-β and the downregulation of PTEN. The present findings suggested that miR-10b might be a potential therapeutic target for esophageal cancer.

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Section: Discussionsupporting

confidence: 65%

Effect and mechanism of microRNA‑10b on proliferation and invasion of esophageal cancer cells

Liu

Salai

et al. 2019

Exp Ther Med

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“…The pleiotropic nature of microRNA-10b was due to its suppression of multiple tumor suppressors, including ras homolog family member C (RhoC), urokinase plasminogen activator receptor (uPAR), matrix metalloproteinases (MMPs), tumor protein p53 (TP53), forkhead box O3 (FOXO3), CYLD lysine 63 deubiquitinase (CYLD), paired box 6 (PAX6), patched 1 (PTCH1), homeobox D10 (HOXD10), notch receptor 1 (NOTCH1), BCL6 transcription repressor (Bcl-6), and Kruppel like factor 4 (KLF4) [29][30][31][32][33]. A recent study reported that microRNA-10b mediated transforming growth factor-β1-regulated glioblastoma proliferation, migration, and epithelial-mesenchymal transition (EMT) [34].…”

Section: Introductionmentioning

confidence: 99%

Deregulation of CSMD1 targeted by microRNA-10b drives gastric cancer progression through the NF-κB pathway

et al. 2019

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Aim:This study aimed to investigate the oncogenic activity of microRNA-10b by targeting CUB and sushi multiple domains protein 1 (CSMD1) in human gastric cancer (GC) and the underlying mechanisms. Methods: The expression of CSMD1 in human GC tissues was evaluated by real-time reverse transcription polymerase chain reaction (RT-PCR), immunoblotting, and immunohistochemical analysis. The expressive abundance of microRNA-10b was detected by stem-loop RT-PCR. Molecular and cellular techniques, including lentiviral vector-mediated knockdown or overexpression, were used to elucidate the effect of microRNA-10b on the expression of CSMD1. Results: CSMD1 was targeted and downregulated by microRNA-10b in human GC tissues and cells, and the down-regulated expression of CSMD1 contributed to poor survival. The knockdown of microRNA-10b expression inhibited cell proliferation in GC cells in vitro and tumor growth in vivo. The inhibition of microRNA-10b expression repressed invasion and migration of HGC27 cells and retarded GC cells metastasis to the liver in Balb/c nude mice. The up-regulated expression of microRNA-10b promoted the proliferation and metastasis of MKN74 cell in vitro. Intratumoral injection of microRNA-10b mimic also promoted the growth and metastasis of tumor xenografts in Balb/c nude mice. Mechanistically, microRNA-10b promoted the invasion and metastasis of human GC cells through inhibiting the expression of CSMD1, leading to the activation of the nuclear factor-κB (NF-κB) pathway that links inflammation to carcinogenesis, subsequently resulting in the upregulation of c-Myc, cyclin D1 (CCND1), and epithelial-mesenchymal transition (EMT) markers. Conclusions: The findings established that microRNA-10b is an oncomiR that drives metastasis. Moreover, a set of critical tumor suppressor mechanisms was defined that microRNA-10b overcame to drive human GC progression.

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“…This multifunctional cytokine of the transforming growth factor b family has been implicated in immunomodulation, proliferation, migration, and epithelial-mesenchymal transition (EMT) of tumor cells [ 18 ]. TGFB1 is also a well-known factor capable of increasing GBM cell proliferation and migration [ 19 – 22 ]. Given that autocrine TGFB1 signaling is essential to sustain stemness and high tumorigenicity of GBM-initiating cells [ 23 ], possible paracrine effects of cytokines released by resident MSC in the tumor stroma must be addressed.…”

Section: Introductionmentioning

confidence: 99%

Mesenchymal stem cells enhance tumorigenic properties of human glioblastoma through independent cell-cell communication mechanisms

et al. 2018

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Mesenchymal stem cells (MSC) display tumor tropism and have been addressed as vehicles for delivery of anti-cancer agents. As cellular components of the tumor microenvironment, MSC also influence tumor progression. However, the contribution of MSC in brain cancer is not well understood since either oncogenic or tumor suppressor effects have been reported for these cells. Here, MSC were found capable of stimulating human Glioblastoma (GBM) cell proliferation through a paracrine effect mediated by TGFB1. Moreover, when in direct cell-cell contact with GBM cells, MSC elicited an increased proliferative and invasive tumor cell behavior under 3D conditions, as well as accelerated tumor development in nude mice, independently of paracrine TGFB1. A secretome profiling of MSC-GBM co-cultures identified 126 differentially expressed proteins and 10 proteins exclusively detected under direct cell-cell contact conditions. Most of these proteins are exosome cargos and are involved in cell motility and tissue development. These results indicate a dynamic interaction between MSC and GBM cells, favoring aggressive tumor cell traits through alternative and independent mechanisms. Overall, these findings indicate that MSC may exert pro-tumorigenic effects when in close contact with tumor cells, which must be carefully considered when employing MSC in targeted cell therapy protocols against cancer.

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MicroRNA-10b mediates TGF-β1-regulated glioblastoma proliferation, migration and epithelial-mesenchymal transition

Cited by 43 publications

References 46 publications

Effect and mechanism of microRNA‑10b on proliferation and invasion of esophageal cancer cells

Effect and mechanism of microRNA‑10b on proliferation and invasion of esophageal cancer cells

Deregulation of CSMD1 targeted by microRNA-10b drives gastric cancer progression through the NF-κB pathway

Mesenchymal stem cells enhance tumorigenic properties of human glioblastoma through independent cell-cell communication mechanisms

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