MicroRNA-424 Predicts a Role for β-1,4 Branched Glycosylation in Cell Cycle Progression

Vaiana, Christopher A.; Kurćon, Tomasz; Mahal, Lara K.

doi:10.1074/jbc.m115.672220

Cited by 26 publications

(43 citation statements)

References 47 publications

(62 reference statements)

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“…Mechanistic studies from cell lines and animal model with regard to miR‐424 have identified several down‐stream targets or signaling pathways/axes in cancers, including Akt3/E2F3 and c‐Myc in HCC, DNMT1 in bladder cancer , MGAT4A , E2F7 in endometrial carcinoma, BCR‐ABL in chronic myeloid leukemia , and EMT–MET axes in breast cancer . Mechanistically, we for the first time identified that YAP1 was a direct down‐stream target of miR‐424‐3p.…”

Section: Discussionmentioning

confidence: 81%

Loss of MiR‐424‐3p, not miR‐424‐5p, confers chemoresistance through targeting YAP1 in non‐small cell lung cancer

Zhang

Zeng

Zhao

et al. 2016

Molecular Carcinogenesis

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MiR-424 has been discovered to be involved in the chemoresistance of lung cancer. However, the underlying mechanism by which miR-424 played role in chemoresistance has been unknown. Here, in our study, to investigate the role of miR-424 in non-small cell lung cancer (NSCLC), we have detected the expression of miR-424-3p and -5p in NSCLC tissues and paired normal control. Moreover, to explore the role of miR-424-3p in NSCLC cells, miR-424-3p and -5p were both re-expressed and knocked down using transient transfection with their respective mimics and inhibitors. Cell viability, migration, and invasion were evaluated using MTT, wound-healing and Transwell assays, respectively. It was found that down-regulation of miR-424-3p was pronouncedly associated with NSCLC progression and overall prognosis; and that both miR-424-3p and -5p were markedly capable of preventing the proliferation, migration, and invasion in NSCLC cells. Additionally, it is miR-424-3p but not miR-424-5p that enhances the chemo-sensitivity of NSCLC cells through targeting YAP1. Mechanistically, YAP1 was identified as down-stream target of miR-424-3p. Together, it was for the first time in our study found that it is loss of miR-424-3p not miR-424-5p that enables chemoresistance through targeting YAP1 in NSCLC, supporting that miR-424-3p could be used as therapeutic target in the curing of NSCLC with chemoresistance. © 2016 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 81%

Loss of MiR‐424‐3p, not miR‐424‐5p, confers chemoresistance through targeting YAP1 in non‐small cell lung cancer

Zhang

Zeng

Zhao

et al. 2016

Molecular Carcinogenesis

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“…MiR-424 targeted N -acetylglucosaminyltransferase that predicted a role for β -1,4 branched glycosylation in cell cycle progression in multiple mammary epithelial cell lines. 32 MiR-199a targeted ST ST6GAL1 that added an 2, 6-linked sialic acid to the termini of N -linked glycans, and reduced its expression and the sialylation of Necl-2. 33 MiR-200a targeted mRNA levels of ST ST3GAL3 and ST3GAL4, which potentially involved in antithrombin sialylation.…”

Section: Discussionmentioning

confidence: 99%

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

Dong

et al. 2016

Cell Death Dis

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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.

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“…miRNA regulate biological pathways by regulating sets of gene transcripts. Multiple laboratories have demonstrated that downregulation of single glycogene (or other gene) targets of miRNA mimic the biological effects of the miRNA [31–33]. Thus, miRNAs could be used as a proxy to identify glycosylation enzymes involved in the pathways they regulate (miRNA proxy approach) [32,33].…”

Section: Multi-level Regulation Of Glycosylationmentioning

confidence: 99%

“…Multiple laboratories have demonstrated that downregulation of single glycogene (or other gene) targets of miRNA mimic the biological effects of the miRNA [31–33]. Thus, miRNAs could be used as a proxy to identify glycosylation enzymes involved in the pathways they regulate (miRNA proxy approach) [32,33]. The miRNA proxy approach has been applied to identify functionally relevant glycogenes impacting cell states like epithelial-to-mesenchymal transition (EMT) [32] and the cell cycle [33].…”

Section: Multi-level Regulation Of Glycosylationmentioning

confidence: 99%

“…Thus, miRNAs could be used as a proxy to identify glycosylation enzymes involved in the pathways they regulate (miRNA proxy approach) [32,33]. The miRNA proxy approach has been applied to identify functionally relevant glycogenes impacting cell states like epithelial-to-mesenchymal transition (EMT) [32] and the cell cycle [33]. For example, miR-200b, a regulator of EMT, was found to regulate a set of glycogenes from hard to analyze cohorts those involved in glycolipid (ST3GAL5 and ST6GALNAC5) and non-canonical O-glycan biosynthesis (B3GLCT).…”

Section: Multi-level Regulation Of Glycosylationmentioning

confidence: 99%

See 1 more Smart Citation

Multi-level regulation of cellular glycosylation: from genes to transcript to enzyme to structure

Neelamegham

Mahal

2016

Current Opinion in Structural Biology

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Glycosylation is a ubiquitous mammalian post-translational modification that both decorates a majority of expressed proteins and regulates their function. Cellular glycan biosynthesis is facilitated by a few hundred enzymes that are collectively termed ‘glycoenzymes’. The expression and activity of these enzymes is controlled at the transcription, translation and post-translation levels. New wet-lab advances are providing analytical methods to collect large-scale data at these multiple levels, relational databases are starting to collate these results, and computer models are beginning to integrate this information across scales in order to gain new knowledge. These activities are likely to enable the qualitative and quantitative mapping of pathways regulating glycan production and function in proteins, cells and tissue.

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MicroRNA-424 Predicts a Role for β-1,4 Branched Glycosylation in Cell Cycle Progression

Cited by 26 publications

References 47 publications

Loss of MiR‐424‐3p, not miR‐424‐5p, confers chemoresistance through targeting YAP1 in non‐small cell lung cancer

Loss of MiR‐424‐3p, not miR‐424‐5p, confers chemoresistance through targeting YAP1 in non‐small cell lung cancer

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

Multi-level regulation of cellular glycosylation: from genes to transcript to enzyme to structure

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