Control of post-translational modifications in antithrombin during murine post-natal development by miR-200a

Teruel, R.; Martínez‐Martínez, Irene; Guerrero, José Antonio López; Gónzález-Conejero, Rocío; Morena‐Barrio, María Eugenia de la; Salloum-Asfar, Salam; Arroyo, Ana B.; Águila, Sonia; García-Barberá, Nuria; Miñano, Antonia; Vicente, Vicente; Corral, Javier; Martı́nez, Constantino

doi:10.1186/1423-0127-20-29

Cited by 10 publications

(6 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…33 MiR-200a targeted mRNA levels of ST ST3GAL3 and ST3GAL4, which potentially involved in antithrombin sialylation. 34 Our recent results also showed that miR-224-3p directly targeted 3′-UTR of fucosyltransferase FUT4 mRNA and sensitized drug-resistant breast cancer cells to chemotherapeutics and reduced the growth rate of breast cancer xenografts in vivo . 35 …”

Section: Discussionmentioning

confidence: 74%

Functional roles of sialylation in breast cancer progression through miR-26a/26b targeting ST8SIA4

Dong

et al. 2016

Cell Death Dis

View full text Add to dashboard Cite

Sialylation is one of the altered glycosylation patterns associated with cancer progression. In this study, we investigated the N-glycan profiles of breast cancer patients and cell lines to reveal sialylation associated with breast cancer progression, and provided new evidences of miRNA-mediated sialylation. MALDI-TOF MS analysis revealed that N-glycans found in breast cancer tissues and breast cancer cell MDA-MB-231 featured increased levels of sialylation compared with adjacent tissues and normal breast epithelial cell MCF-10A. The expressional profiles of 20 sialyltransferase genes were then analyzed and found significantly different comparing breast cancer samples with adjacent tissues, and two breast cancer cell lines MDA-MB-231 and MCF-7 with different metastatic potential and MCF-10A cells. Tumor tissues and highly metastatic breast cancer cell line MDA-MB-231 exhibited higher levels of ST8SIA4. Knocking down ST8SIA4 in breast cancer cell lines significantly inhibited their malignant behaviors including cell proliferation and invasion in a sialyltransferase-dependent manner. By applying bioinformatic approaches for the prediction of miRNA targeting 3′-UTR of ST8SIA4, we identified ST8SIA4 as one of the miR-26a/26b-targeted genes. Further data analysis revealed the inversely related expression of ST8SIA4 and miR-26a/26b in breast cancer cells, tumor tissues and corresponding adjacent tissues. The ability of miR-26a/26b to interact specifically with and regulate the 3′-UTR of ST8SIA4 was demonstrated via a luciferase reporter assay. The forced expression of miR-26a/26b was able to induce a decrease of ST8SIA4 level and also to affect breast cancer cells progression, while altered expression of ST8SIA4 in breast cancer cells modulated progression upon transfection with miR-26a/26b mimics or inhibiter. Taken together, these results indicate that changes in the glycosylation patterns and sialylation levels may be useful markers of the progression of breast cancer, as well as miR-26a/26b may be widely involved in the regulation of sialylation machinery by targeting ST8SIA4.

show abstract

Section: Discussionmentioning

confidence: 74%

Functional roles of sialylation in breast cancer progression through miR-26a/26b targeting ST8SIA4

Dong

et al. 2016

Cell Death Dis

View full text Add to dashboard Cite

show abstract

“…AT from newborn mice has an incomplete content of sialic acid, which may be explained by the lower expression of two sialyltransferases. Our data suggest that miR‐200a, an miRNA expressed in liver and inversely correlated with the expression of the two sialyltransferases, may be, in part, involved in their regulation . Thus, the role of miRNAs in hemostasis does not seem to be restricted to the direct control of proteins, but could be extended to include indirect effects on elements involved in transcriptional or post‐translational processes.…”

Section: Mirna As a Regulator Of The Hemostatic Systemmentioning

confidence: 87%

“…Indeed, miR‐18a and miR‐19b, two potential regulators of AT in the liver, as predicted by two different and widely used algorithms, were inversely correlated with SERPINC1 mRNA levels during the first 19 days of postnatal development . The regulation may be even more complex, as the qualitative changes observed in AT during development may also be regulated by miRNAs , which may have functional consequences for hemostasis. AT from newborn mice has an incomplete content of sialic acid, which may be explained by the lower expression of two sialyltransferases.…”

Section: Mirna As a Regulator Of The Hemostatic Systemmentioning

confidence: 99%

MicroRNAs in hemostasis

Teruel‐Montoya

Rosendaal

Martı́nez

2015

Journal of Thrombosis and Haemostasis

View full text Add to dashboard Cite

To cite this article: Teruel-Montoya R, Rosendaal FR, Mart ınez C. MicroRNAs in hemostasis. J Thromb Haemost 2015; 13: 170-81.Summary. Epidemiologic studies have revealed that modification of the levels of individual components of the hemostatic system may have effects on the development of thrombosis or hemorrhage. To maintain the necessary equilibrium, the hemostatic system is finely regulated. It is known that acquired factors and/or alterations in genes (single-nucleotide polymorphisms or mutations) may be the cause of interindividual differences or exacerbated levels of hemostatic proteins in plasma, but there are still many non-characterized factors that provoke such variations. The search for new elements, such as microRNAs (miRNAs), a family of small non-coding RNAs that are novel regulators of protein expression, may reveal an additional layer at which to investigate the causes of hemostatic diseases. In this review, we discuss the latest developments in research into the role of miRNAs in the regulation of several hemostatic factors, and the potential use of miRNAs as prognostic or diagnostic tools in hemostasis and thrombosis.

show abstract

“…Vaiana et al demonstrated that MGAT4A, an N-acetylglucosamintltransferase that installed the β-1, 4 branch of N-glycans, was directly regulated by miR-424 in multiple mammary epithelial cell lines [ 31 ]. MiR-200a might target ST3GAL3 and ST3GAL4 sialyltransferases, which potentially involved in antithrombin sialylation, were 85% lower in neonates in comparison with adults [ 32 ]. MiR-199a targeted ST6GAL1 and reduced both the sialylation and the protein level of Necl-2 [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Upregulation of miR-181c inhibits chemoresistance by targeting ST8SIA4 in chronic myelocytic leukemia

Zhao

Song

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Chemotherapy resistance frequently drives tumor progression. Increased expression of ST8SIA4 has been reported in diverse carcinomas and highly correlates with leukemia multidrug resistance (MDR). MicroRNAs (miRNA) are widely recognized as key players in cancer progression and drug resistance. Here, to explore whether miRNA modulates the sensitivity of chronic myelocytic leukemia (CML) to chemotherapeutic agents and regulates ST8SIA4 expression, we analyzed the complete miRNA expression profile and found a subset of miRNAs specifically dysregulated in adriamycin-resistant CML cell line K562/ADR and its parent cell line K562. Compared with three pairs of CML cell lines and 38 clinical samples of peripheral blood mononuclear cells (PBMC) of CML patients, miR-181c expression was down-regulated in drug-resistant cell lines and CML/MDR samples. Altered expression levels of miR-181c influenced the MDR phenotypes of K562 and K562/ADR. Reporter-gene assay showed that miR-181c directly targeted and inhibited the ST8SIA4 expression, as well as miR-181c was inversely correlated with the levels of ST8SIA4 expression in CML cell lines and samples. Moreover, ST8SIA4 could reverse the effect of miR-181c on drug resistance in K562 and K562/ADR cells in vitro. Upregulation of miR-181c sensitized K562/ADR cells to adriamycin in vivo through directly suppressing ST8SIA4 expression. Further investigation showed that miR-181c mediated the activity of phosphoinositide-3 kinase (PI3K)/AKT signal pathway, and inhibition of PI3K/Akt in K562 cells counteracted miR-181c-mediated MDR phenotype. These data revealed an important role for miR-181c in the regulation of chemoresistance in CML, and suggested the potential application of miR-181c in drug resistance treatment.

show abstract

Control of post-translational modifications in antithrombin during murine post-natal development by miR-200a

Cited by 10 publications

References 34 publications

Functional roles of sialylation in breast cancer progression through miR-26a/26b targeting ST8SIA4

Functional roles of sialylation in breast cancer progression through miR-26a/26b targeting ST8SIA4

MicroRNAs in hemostasis

Upregulation of miR-181c inhibits chemoresistance by targeting ST8SIA4 in chronic myelocytic leukemia

Contact Info

Product

Resources

About