MiR-513c suppresses neuroblastoma cell migration, invasion, and proliferation through direct targeting glutaminase (GLS)

Xia, Hongliang; Lv, Yao; Xu, C.; Fu, Mingcui; Zhang, Ting; Yan, Xiao; Dai, Shu-Ho; Xiong, Qianwei; Zhou, Yun; Wang, Jian; Cao, Xu

doi:10.3233/cbm-170577

Cited by 31 publications

(29 citation statements)

References 20 publications

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“…The Streicher's group indicated that in cutaneous melanoma, the miR-506-514 cluster was consistently overexpressed and mediated the melanocytes transformation [37]. On the other hand, it has been shown that the downregulation of hsa-miR-513c promotes the proliferation and invasiveness of neuroblastoma and glioma cells [38,39]. Similar to that downregulation of hsa-miR-506, leads to increased proliferation, invasiveness, and epithelial to mesenchymal transition in breast gastric and ovarian cancer [40][41][42].…”

Section: Discussionmentioning

confidence: 97%

The Potential Role of Selected miRNA in Uveal Melanoma Primary Tumors as Early Biomarkers of Disease Progression

Wróblewska

Lach

Ustaszewski

et al. 2020

Genes

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Uveal melanoma (UM) is the most common primary tumor of the eye diagnosed in adults, associated with a high risk of metastasis and thereby, poor prognosis. Among known risk factors for the development of metastatic disease is the loss of BAP1 expression and chromosome 3 monosomy in the primary tumor. However, the expression levels of specific micro RNAs (miRNA) in tumor tissue may also serve as a valuable marker for determining the risk of metastatic disease in patients with primary uveal melanoma. In our study, we analyzed the miRNA expression data of cases selected from The Cancer Genome Atlas study on uveal melanoma, and determined a panel of 15 miRNAs differentially expressed between patients with primary and metastatic disease. Next, 6 miRNAs were validated on a group of 46 tumor samples from primary and metastatic patients. We have shown, that expression of hsa-miR-592, hsa-miR-346, and hsa-miR-1247 was significantly increased, while hsa-miR-506 and hsa-miR-513c were decreased in the tumors of patients with metastatic disease. Hsa-miR-196b expression did not differ between the two subgroups, however, we showed significant correlation with BAP1 expression. Moreover, hsa-miR-592 also showed correlation with monosomy 3 tumors. Gene ontology analysis revealed involvement of those miRNAs with cellular processes mediating the metastatic process. Our results showed that miRNAs play an important role in the deregulation of several oncogenic pathways in UM and can, thereby, promote metastatic spread to distant organs. Moreover, differentially expressed miRNAs may be used as an interesting biomarker for the assessment of metastatic risk in uveal melanoma patients.

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Section: Discussionmentioning

confidence: 97%

The Potential Role of Selected miRNA in Uveal Melanoma Primary Tumors as Early Biomarkers of Disease Progression

Wróblewska

Lach

Ustaszewski

et al. 2020

Genes

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“…In addition, miR‐204 may also be involved in the chondrogenic differentiation of periodontal ligament stem cells . miR‐513c was reported to inhibit the development of nervous system tumours and hepatocellular carcinoma . Nevertheless, little research has been conducted to reveal their roles in periodontal inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…64 miR-513c was reported to inhibit the development of nervous system tumours and hepatocellular carcinoma. [65][66][67] Nevertheless, little research has been conducted to reveal their roles in periodontal inflammation.…”

Section: Discussionmentioning

confidence: 99%

Assessment of microRNA‐144‐5p and its putative targets in inflamed gingiva from chronic periodontitis patients

Wang

Chen

et al. 2018

J of Periodontal Research

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Background and Objective This study aimed to discover the distinctive MicroRNAs (miRNA) functioning in the pathogenesis of periodontal inflammation, which might be potential therapy targets of chronic periodontitis. Material and Methods miRNA profiles of human inflamed gingival tissue from three previous microarrays were re‐analysed. Gingival tissues were collected for the validation of overlapping miRNAs, and a network was constructed to show regulatory connection between overlapping miRNAs and periodontitis‐associated target genes. Potential miRNAs were screened based on their expression levels and predicted target genes. Correlation analysis and binding site prediction were conducted to reveal the relationship between the potential miRNAs and their target genes. Results miR‐144‐5p, found to be upregulated in all three studies, showed the greatest upregulation (P < 0.0001). Another 16 miRNAs (10 upregulated and six downregulated) overlapped between any two of the three studies. All overlapping miRNAs had expected expression levels except for miR‐203 during validation. Ten miRNAs (six upregulated and four downregulated) were found to have periodontal inflammation‐associated targets. Cyclooxygenase 2 (COX2) and interleukin‐17F (IL17F), predicted target genes of upregulated miR‐144‐5p, showed significant decreases and were negatively correlated with miR‐144‐5p in the periodontitis group (r = −0.742 for COX2, r = −0.615 for IL17F). Conclusion This re‐analysis of miRNA signatures has implied the potential regulatory mechanism of miR‐144‐5p and its potential for exploring alternative therapeutic approaches, especially those that use miRNA delivery systems to treat chronic periodontitis. Nevertheless, further study based on larger sample size and homogenous cells is needed to reveal the exact roles of miRNAs in chronic periodontitis.

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“…This effect was attributed to the decrease in GLS mRNA, since it is a direct target of miR-513c. These findings suggest that miR-513c may act as a tumor suppressor and deserves to be studied for consideration in neuroblastoma treatment [114] (Figure 2).…”

Section: Mir-513cmentioning

confidence: 97%

Non-Coding RNAs as Key Regulators of Glutaminolysis in Cancer

Ortiz-Pedraza

Muñoz-Bello

Olmedo-Nieva

et al. 2020

IJMS

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Cancer cells exhibit exacerbated metabolic activity to maintain their accelerated proliferation and microenvironmental adaptation in order to survive under nutrient-deficient conditions. Tumors display an increase in glycolysis, glutaminolysis and fatty acid biosynthesis, which provide their energy source. Glutamine is critical for fundamental cellular processes, where intermediate metabolites produced through glutaminolysis are necessary for the maintenance of mitochondrial metabolism. These include antioxidants to remove reactive oxygen species, and the generation of the nonessential amino acids, purines, pyrimidines and fatty acids required for cellular replication and the activation of cell signaling. Some cancer cells are highly dependent on glutamine consumption since its catabolism provides an anaplerotic pathway to feed the Krebs cycle. Intermediate members of the glutaminolysis pathway have been found to be deregulated in several types of cancers and have been proposed as therapeutic targets and prognostic biomarkers. This review summarizes the main players in the glutaminolysis pathway, how they have been found to be deregulated in cancer and their implications for cancer maintenance. Furthermore, non-coding RNAs are now recognized as new participants in the regulation of glutaminolysis; therefore, their involvement in glutamine metabolism in cancer is discussed in detail.Int. J. Mol. Sci. 2020, 21, 2872 2 of 26 an increased glucose consumption in relation to normal differentiated tissues. Now we know that glutamine metabolism is as important as glucose metabolism for the production of macromolecules in cancer [1].Glutamine is an abundant amino acid involved in energy production, homeostasis in pro/antioxidant species and the activation of signaling pathways in cancer. In addition to the antioxidant glutathione (GSH), nucleotides, lipids and amino acids are formed from glutamine metabolism. All of these are needed for many metabolic functions such as growth, proliferation, cell survival and defense against oxidative stress [2]. Glutamine contributes, with reduced nitrogen, to the de novo biosynthesis of diverse nitrogen-containing compounds, such as purine and pyrimidine nucleotides, glucosamine-6-phosphate and nonessential amino acids.As glutamine is the most abundant amino acid in the blood and muscle tissue, normal proliferating cells use glutamine metabolism as an energy source, mediated by its catabolic products, glutamate and α-ketoglutarate (α-kG), the latter being an intermediate of the tricarboxylic acid cycle (TCA) or Krebs cycle [3]. In 1950, Harry Eagle observed that HeLa tumor cells require an excess of glutamine, in relation to other amino acids in the culture medium, for optimal growth. Furthermore, it has been reported that tumors consume glutamine faster than the surrounding normal tissue [4]. Moreover, most cancer cells are dependent on glutamine being unable to survive under glutamine starvation, an effect that has been termed glutamine addiction [5]. Various types of cancers are high...

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MiR-513c suppresses neuroblastoma cell migration, invasion, and proliferation through direct targeting glutaminase (GLS)

Cited by 31 publications

References 20 publications

The Potential Role of Selected miRNA in Uveal Melanoma Primary Tumors as Early Biomarkers of Disease Progression

The Potential Role of Selected miRNA in Uveal Melanoma Primary Tumors as Early Biomarkers of Disease Progression

Assessment of microRNA‐144‐5p and its putative targets in inflamed gingiva from chronic periodontitis patients

Non-Coding RNAs as Key Regulators of Glutaminolysis in Cancer

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