MiR-124 represses vasculogenic mimicry and cell motility by targeting amotL1 in cervical cancer cells

Wan, Haisu; Li, Qin‐Qin; Zhang, Yan; Tian, Wei; Li, Yanan; Liu, Min; Li, Xin; Tang, Hua

doi:10.1016/j.canlet.2014.09.005

Cited by 91 publications

(81 citation statements)

References 42 publications

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“…Zhao et al [49] showed that miR-186 regulates prostate cancer VM formation via targeting Twist1. In addition, Wan et al [50] demonstrated that miR-124 overexpression suppresses VM formation by inhibiting amotL1 expression in cervical cancer cells. Moreover, miR-26b [51], miR-9 [52], and miR-let-7f [53] were reported to inhibit glioma VM formation.…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis

Gao

Liu

et al. 2017

Cell Physiol Biochem

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Background/Aims: Vasculogenic mimicry (VM) has been reported to be a novel glioma neovascularization process. Anti-VM therapy provides new insight into glioma clinical management. In this study, we revealed the role of the long non-coding RNA HOXA cluster antisense RNA 2 (HOXA-AS2) in malignant glioma behaviors and VM formation. Methods: Quantitative real-time PCR was performed to determine the expression levels of HOXA-AS2 in glioma samples and glioblastoma cell lines. CD34-periodic acid-Schiff dual-staining was performed to assess VM in glioma samples. CCK-8, transwell, and Matrigel tube formation assays were performed to measure the effects of HOXA-AS2 knockdown on cell viability, migration, invasion, and VM tube formation, respectively. RNA immunoprecipitation, dual-luciferase reporter and Western blot assays were performed to explore the molecular mechanisms underlying the functions of HOXS-AS2 in glioblastoma cells. A nude mouse xenograft model was used to investigate the role of HOXA-AS2 in xenograft glioma growth and VM density. Student’s t-tests, one-way ANOVAs followed by Bonferroni posthoc tests, and chi-square tests were used for the statistical analyses. Results: HOXA-AS2 was upregulated in glioma samples and cell lines and was positively correlated with VM. HOXA-AS2 knockdown attenuated cell viability, migration, invasion, and VM formation in glioma cells and inhibited the expression of vascular endothelial-cadherin (VE-cadherin), as well as the expression and activity of matrix metalloproteinase matrix metalloproteinase (MMP)-2 and MMP-9. miR-373 was downregulated in glioma samples and cell lines and suppressed malignancy in glioblastoma cells. HOXA-AS2 bound to miR-373 and negatively regulated its expression. Epidermal growth factor receptor (EGFR), a target of miR-373, increased the expression levels of VE-cadherin, as well as the expression and activity levels of MMP-2 and MMP-9, via activating phosphatidylinositol 3-kinase/serine/threonine kinase pathways. HOXA-AS2 knockdown combined with miR-373 overexpression yielded optimal tumor suppressive effects and the lowest VM density in vivo. Conclusion: HOXA-AS2 knockdown inhibited malignant glioma behaviors and VM formation via the miR-373/EGFR axis.

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Section: Discussionmentioning

confidence: 99%

Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis

Gao

Liu

et al. 2017

Cell Physiol Biochem

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“…Simultaneously, miRNA-27a was demonstrated to be involved in modulating drug resistance mediated by MDR1/Pglycoprotein in ovarian cancer cells [6]. In recent years, miR-124 has been a focus of interest for its role as a tumor suppressor in the development of several types of cancers, such as prostate cancer, cervical cancer, colorectal cancer, and so on [7][8][9]. Moreover, CpG island methylation-mediated downregulation of miR-124 has been determined to be associated with poor prognosis and disease recurrence in patients with clear cell renal cell carcinoma [10].…”

Section: Introductionmentioning

confidence: 98%

miR-124 represses FZD5 to attenuate P-glycoprotein-mediated chemo-resistance in renal cell carcinoma

Long

Liu

et al. 2015

Tumor Biol.

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Renal cell carcinoma (RCC) is one of most malignant neoplasms, exhibiting poor responsiveness to the conventional chemo-regime. Abnormal expression of P-glycoprotein (P-gp) has been implicated in the emergence of multiple-drug resistance (MDR) by reducing the accumulation of intracellular chemotherapy drugs. Wnt signaling plays critical roles in renal cancer and is triggered by binding of Wnt ligands to Frizzled (FZD) receptor proteins. miR-124 is a tumor suppressor associated with cancer relapse and MDR, whereas its role in P-gp-mediated MDR in refractory RCC is as yet unrevealed. Our study aimed to investigate the roles of miR-124 in chemo-resistant RCC cells and the potential targeted signaling paths in inducing P-gp expression. Doxorubicin (DOX)- and vinblastine (VBL)-resistant Caki-2 cells were developed by exposure of parental Caki-2 cells to the agents over a long period of time. In comparison with their parental cells, miR-124 was downregulated in Caki-2/DOX and Caki-2/VBL cells, accompanied by increased FZD5 and P-gp. IC50 values were reduced significantly after miR-124 mimics were introduced into Caki-2/DOX cells. In addition, miR-124 mimics significantly promoted apoptosis of Caki-2/DOX cells. miR-124 targeted to FZD5 and miR-124 mimics as well as FZD5 siRNA showed significant inhibitory effects on P-gp expression in Caki-2/DOX cells. Furthermore, Wnt-5a dose-dependently stimulated the presentation of p-PKCα/βII and p-CamKII via activating FZD5, which was reversed by FZD5 silencing. Moreover, FZD5/protein kinase C (PKC) signaling is responsible for the elevation of P-gp and cancer cell survival. In conclusion, restoring miR-124 may function as a promising strategy to overcome P-gp-mediated MDR by inhibiting FZD5/PKC signaling.

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“…Details of the procedure of MTT, colony formation, and invasion assays can be found in Long et al [2012] and Wan et al [2014].…”

Section: Mtt Colony Formation and Invasion Assaysmentioning

confidence: 99%

“…BCL6 sense, 5′-TC-CTCGGAAGATGAGATTGC-3′, BCL6 antisense, 5′-GTTGAG-CACGATGAACTTGTA-3′; β-actin sense, 5′-CTACGTC-GCCCTGGACTTCGAGC-3′; and β-actin antisense, 5′-GATG-GAGCCGCCGATCCACACGG-3′. The details of the experimental protocol of RNA extraction and RT-qPCR can be found in Wan et al [2014].…”

Section: Rt-qpcrmentioning

confidence: 99%

miR-519d-3p Inhibits Cell Proliferation and Invasion of Gastric Cancer by Downregulating B-Cell Lymphoma 6

Shao²,

Zhang³

et al. 2018

Cytogenet Genome Res

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miR-519d inhibits cell growth, migration, and invasion, but its role in gastric cancer (GC) cells is obscure. We showed that miR-519d-3p was lowly expressed in GC tissues and was associated with the clinical stage and lymph node metastasis of GC tissues. We found that miR-519d-3p repressed cell proliferation and invasion of MGC803 cells and delayed the G1/S phase transition, resulting in decreased cyclin B1 and MMP2 and increased E-cadherin levels. Furthermore, miR-519d-3p targeted and downregulated B-cell lymphoma 6 (BCL6) expression. BCL6 overexpression partially abrogated the suppressive function of miR-519d in MGC803 cells. In conclusion, our study demonstrated that miR-519d-3p functions as a tumor suppressor by targeting and downregulating the expression of BCL6 in GC cells.

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MiR-124 represses vasculogenic mimicry and cell motility by targeting amotL1 in cervical cancer cells

Cited by 91 publications

References 42 publications

Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis

Long Non-Coding RNA HOXA-AS2 Regulates Malignant Glioma Behaviors and Vasculogenic Mimicry Formation via the MiR-373/EGFR Axis

miR-124 represses FZD5 to attenuate P-glycoprotein-mediated chemo-resistance in renal cell carcinoma

miR-519d-3p Inhibits Cell Proliferation and Invasion of Gastric Cancer by Downregulating B-Cell Lymphoma 6

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