MicroRNA‐1 (miR‐1) inhibits chordoma cell migration and invasion by targeting slug

Osaka, Eiji; Yang, Xiaoqian; Shen, Jacson K.; Yang, Pei; Feng, Yong; Mankin, Henry J.; Hornicek, Francis J.; Duan, Zhenfeng

doi:10.1002/jor.22632

Cited by 43 publications

(32 citation statements)

References 32 publications

(57 reference statements)

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“…Western blot analyses were carried out as previously described. 25 Membrane signals were scanned using the Odyssey infrared imaging system and analyzed using Odyssey 3.0 software (LI-COR Biosciences). Relative expression values were normalized assigning the value of the cells in control groups to 1.0.…”

Section: Methodsmentioning

confidence: 99%

Targeting Cdk11 in osteosarcoma cells using the CRISPR‐cas9 system

Feng

Sassi

Shen

et al. 2014

Journal Orthopaedic Research

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Osteosarcoma is the most common type primary malignant tumor of bone. Patients with regional osteosarcoma are routinely treated with surgery and chemotherapy. In addition, many patients with metastatic or recurrent osteosarcoma show poor prognosis with current chemotherapy agents. Therefore, it is important to improve the general condition and the overall survival rate of patients with osteosarcoma by identifying novel therapeutic strategies. Recent studies have revealed that CDK11 is essential in osteosarcoma cell growth and survival by inhibiting CDK11 mRNA expression with RNAi. Here, we apply the Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-Cas9 system, a robust and highly efficient novel genome editing tool, to determine the effect of targeting endogenous CDK11 gene at the DNA level in osteosarcoma cell lines. We show that CDK11 can be efficiently silenced by CRISPR-Cas9. Inhibition of CDK11 is associated with decreased cell proliferation and viability, and induces cell death in osteosarcoma cell lines KHOS and U-2OS. Furthermore, the migration and invasion activities are also markedly reduced by CDK11 knockout. These results demonstrate that CRISPR-Cas9 system is a useful tool for the modification of endogenous CDK11 gene expression, and CRISPR-Cas9 targeted CDK11 knockout may be a promising therapeutic regimen for the treatment of osteosarcoma.

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Section: Methodsmentioning

confidence: 99%

Targeting Cdk11 in osteosarcoma cells using the CRISPR‐cas9 system

Feng

Sassi

Shen

et al. 2014

Journal Orthopaedic Research

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“…[7][8][9][10] More importantly, LDHA silencing could increase apoptosis and suppress metastasis in a series of cancer cells. 14,15 Recently, accumulating studies show that dysregulated miRNAs play important roles in regulating cellular metabolism in various human malignancies including GBC. Nevertheless, the expression level and role of LDHA in GBC have not been reported.…”

Section: Introductionmentioning

confidence: 99%

LDHA is a direct target of miR‐30d‐5p and contributes to aggressive progression of gallbladder carcinoma

Chen

et al. 2018

Molecular Carcinogenesis

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Gallbladder cancer (GBC) is the most general biliary tract malignancy, with poor prognosis due to rapid tumor progression and lack of specific symptoms. Lactate dehydrogenase-A (LDHA) can promote Warburg effect to produce lactate and Adenosine Triphosphate (ATP) in aerobic condition, which contributes to oncogenesis metastasis and drug resistance in various cancers. However, the expression and functional role of LDHA in GBC are largely unknown. We determined that LDHA was over-expressed in GBC tumor tissues compared with normal tissues, which was also an independent prognostic factor for the overall survival of GBC patients by tissue microarrays analysis. In addition, RNAi-mediated LDHA silencing could suppress the GBC cell proliferation, invasion, colony formation and glycolysis while promoting cell apoptosis in vitro. Similar results were observed in GBC cells treated with LDHA specific inhibitor FX11. Moreover, we confirmed that knockdown of LDHA could inhibit tumor growth in vivo. Additionally, we found that the 3'-untranslated region (3'-UTR) of LDHA mRNA was the direct target of microRNA-30d-5p (miR-30d-5p), which was low expressed in GBC tissues and associated with poor prognosis of GBC patients. Our findings disclose a novel role for miR-30d-5p/LDHA axis contribute to aggressive progression by reprogramming the metabolic process in GBC cells, and suggest a potential application of miR-30d-5p/LDHA axis in prognosis prediction and GBC treatment.

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“…For example, reduced expression of miR-1 has been reported in chordoma, and miR-1 is suggested to suppress the growth of chordoma cells by inhibiting Met and histone deacetylase 4 (17). Further studies have shown that miR-1 inhibits chordoma cell migration and invasion and correlates with clinical prognosis (18,19). Another study confirmed that miR-608 and miR-34a were significantly downregulated in chordoma and may influence chordoma malignancy by targeting epidermal growth factor receptor (EGFR), B-cell lymphoma-xL and Met (20).…”

Section: Discussionmentioning

confidence: 99%

miR-219-5p inhibits proliferation and clonogenicity in chordoma cells and is associated with tumor recurrence

et al. 2016

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Chordoma is a rare malignant bone tumor that is usually localized to the skull base, vertebral column and sacrum. The transcription factor brachyury, which is encoded by the T gene, has a critical role in the development and progression of chordoma, although the mechanisms underlying brachyury regulation remain unclear. The aim of the current study was to identify and characterize microRNAs (miRs) that regulate brachyury expression in chordoma. MicroRNAs that target brachyury were predicted using miRanda and TargetScan. Using reverse transcription-quantitative polymerase chain reaction, miR-219-5p was shown to be significantly downregulated in chordoma tissues and the U-CH2 chordoma cell lines. A dual-luciferase reporter assay was used to validate the inhibitory effect of miR-219-5p on brachyury mRNA expression. The expression level of brachyury was downregulated in U-CH2 cells following transfection with miR-219-5p mimics and upregulated following transfection with the miR-219-5p inhibitor. The effects of miR-219-5p on the proliferation and clonogenicity of chordoma cells were assessed using cell counting kit-8, EdU and clone formation assays. These in vitro results indicated that miR-219-5p may have an important role in regulating the cell proliferation and clonogenicity of human chordoma cells, potentially by targeting brachyury. Furthermore, the associations between the expression levels of miR-219-5p and various clinicopathological factors were analyzed, and miR-219-5p expression was shown to correlate with tumor extent and recurrence. These results suggested that miR-219-5p functions as a tumor suppressor in chordoma and, therefore, that miR-219-50 may be a potential target for therapeutic intervention.

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MicroRNA‐1 (miR‐1) inhibits chordoma cell migration and invasion by targeting slug

Cited by 43 publications

References 32 publications

Targeting Cdk11 in osteosarcoma cells using the CRISPR‐cas9 system

Targeting Cdk11 in osteosarcoma cells using the CRISPR‐cas9 system

LDHA is a direct target of miR‐30d‐5p and contributes to aggressive progression of gallbladder carcinoma

miR-219-5p inhibits proliferation and clonogenicity in chordoma cells and is associated with tumor recurrence

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