Regulation of miR-483-3p by the O-linked N-acetylglucosamine transferase links chemosensitivity to glucose metabolism in liver cancer cells

Pepe, Felice; Pagotto, Sara; Soliman, Shimaa; Rossi, Cláudia; Lanuti, Paola; Braconi, Chiara; Mariani-Costantini, Renato; Visone, Rosa; Veronese, Angelo

doi:10.1038/oncsis.2017.35

Cited by 38 publications

(29 citation statements)

References 31 publications

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“…Moreover, they identified that cellular glucose availability is participated in the regulation of miR-483-3p and demonstrated OGT activity as a molecular mechanisms link between miR-483-3p expression and glucose. Combined with their earlier research results, the glucose/OGT/miR-483-3p signaling pathway plays a vital part in the tumorgenic mechanisms of liver cancer and may involve in the drug resistance 68 . The DLC-1 gene has been revealed as a candidate tumor suppressor, and in colorectal cancer, miR-483-3p contributes to cancer cells proliferation via suppressing its target DLC-1 gene 23 .…”

Section: The Pathways and Interactions Of Mir-483 Involved In Digestimentioning

confidence: 75%

Role of miR-483 in digestive tract cancers: from basic research to clinical value

Zhou¹,

Yang²,

Ma³

et al. 2018

J. Cancer

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Digestive tract cancers (DTCs) is the most common malignant tumors in the world. Despite surgery and medical technology have witnessed the increasing development and sharp advancement in the past decade, DTCs remain a critical concern with high morbidity and mortality. Since a class of small noncoding RNAs termed miRNAs were identified several years ago, increasing studies have attempted to illustrate the relationship between the specific miRNAs dysregulated expression levels and the diseases phenotypic changes. For example, microRNA-483 (miR-483) aberrant expression plays a pivotal part in tumor biology in a variety of human cancer, including DTCs. In this review, we focus on the present key findings from recent profiling studies, discuss the use of miR-483 as a novel biomarker for DTCs. At the same time, we emphasize the significant diversities and technical difficulties must be overcome before clinically relevant signatures arose. It is believed that this might provide researchers an insight into the molecular targeting cancer treatment.

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Section: The Pathways and Interactions Of Mir-483 Involved In Digestimentioning

confidence: 75%

Role of miR-483 in digestive tract cancers: from basic research to clinical value

Zhou¹,

Yang²,

Ma³

et al. 2018

J. Cancer

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“…Interestingly, it has been reported that mature miR-483-3p is upregulated in some types of tumours [32], but downexpressed in others [33]. For example, silencing of miR-483-3p promotes acquired gefitinib resistance and EMT in EGFR-mutant NSCLC by targeting integrin b3 [34], whereas glucose uptake increases the expression of the oncogenic miR-483-3p through the OGT pathway in liver cancer cells [17], suggesting that miR-483-3p may have complicated cancer-type specific functions. However, whether miR-483-3p is involved in oxaliplatin resistance has not been elucidated in colorectal cancer.…”

Section: Discussionmentioning

confidence: 99%

“…In this study, we comparatively assessed differentially expressed miRNAs and genes of HCT116 and HCT116/L cells with the final aim of clarifying the miRNAs and their target genes associated with oxaliplatin resistance. Previous studies have suggested that miR-483-3p was dysregulated in some types of tumours [17][18][19]. However, the mechanisms by which miR-483-3p is associated with oxaliplatin resistance in CRC are largely unknown.…”

Section: Introductionmentioning

confidence: 99%

MiR-483-3p regulates oxaliplatin resistance by targeting FAM171B in human colorectal cancer cells

Liang

Qiang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Oxaliplatin resistance limits the efficiency of treatment for colorectal cancer (CRC). Studies have shown that abnormal expression of microRNAs (miRNAs) were associated with tumorigenesis, cancer development and chemoresistance. The purpose of this study was to identify potential miRNAs related to oxaliplatin resistance in CRC cells. In this work, using small RNA sequencing (small RNA-Seq) and transcriptome sequencing (RNA-Seq), we found that down-regulated miR-483-3p was concurrent with up-regulated FAM171B in oxaliplatin-resistant colorectal cancer cell line HCT116/L as compared with its parental cell line HCT116. Transient transfection of miR-483-3p mimics markedly decreased the levels of FAM171B and restored oxaliplatin responsiveness of HCT116/L cells, and this alteration enhanced cell apoptosis and weakened cell migration. Whereas miR-483-3p inhibitor dramatically promoted the expression of FAM171B and enhanced oxaliplatin resistance of HCT116 cells by repressing cell apoptosis. Furthermore, knockdown of FAM171B in HCT116/L cells could also sensitize its reaction of the treatment with oxaliplatin, which was verified by the reduced cell migration. These findings demonstrate that FAM171B is a functional target of miR-483-3p in the regulation of oxaliplatin resistance in human CRC cells.

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“…OGT silencing increases the sensitivity to 5-FU of BCG-823 gastric cancer cell line by enhancing expression of p53 upregulated modulator of apoptosis (PUMA) and caspase-3 pro-apoptotic proteins [ 159 ]. In this sense, Pepe et al showed in HepG2 hepatoblastoma cells that OGT stabilizes the transcriptional complex β-catenin/upstream stimulatory factor 1 (USF1) at the promoter of miR-483-3p, a microRNA responsible for transcription downregulation of PUMA [ 160 ]. Treatment with 2-deoxy-D-glucose (2-DG), a glucose-mimic inhibitor of glycolysis, reduces miR-483-3p expression and increases sensitivity to 5-FU-induced apoptosis.…”

Section: Glycosylation Alterations In Colorectal Cancer Cells and Resmentioning

confidence: 99%

Drug resistance related to aberrant glycosylation in colorectal cancer

2017

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Colorectal cancer (CRC) is the fourth leading cause of cancer-related deaths in the world. Drug resistance of tumour cells remains the main challenge toward curative treatments efficiency. Several epidemiologic studies link emergence and recurrence of this cancer to metabolic disorders. Glycosylation that modifies more than 80% of human proteins is one of the most widepread nutrient-sensitive post-translational modifications. Aberrant glycosylation participates in the development and progression of cancer. Thus, some of these glycan changes like carbohydrate antigen CA 19-9 (sialyl Lewis a, sLea) or those found on carcinoembryonic antigen (CEA) are already used as clinical biomarkers to detect and monitor CRC. The current review highlights emerging evidences accumulated mainly during the last decade that establish the role played by altered glycosylations in CRC drug resistance mechanisms that induce resistance to apoptosis and activation of signaling pathways, alter drug absorption and metabolism, and led to stemness acquisition. Knowledge in this field of investigation could aid to the development of better therapeutic approaches with new predictive biomarkers and targets tied in with adapted diet.

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Regulation of miR-483-3p by the O-linked N-acetylglucosamine transferase links chemosensitivity to glucose metabolism in liver cancer cells

Cited by 38 publications

References 31 publications

Role of miR-483 in digestive tract cancers: from basic research to clinical value

Role of miR-483 in digestive tract cancers: from basic research to clinical value

MiR-483-3p regulates oxaliplatin resistance by targeting FAM171B in human colorectal cancer cells

Drug resistance related to aberrant glycosylation in colorectal cancer

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