miR-101 Enhances Cisplatin-Induced DNA Damage Through Decreasing Nicotinamide Adenine Dinucleotide Phosphate Levels by Directly Repressing Tp53-Induced Glycolysis and Apoptosis Regulator Expression in Prostate Cancer Cells

Huang, Shiqiao; Yang, Zhiguo; Ma, Yong; Yang, Yiyong; Wang, Shangren

doi:10.1089/dna.2016.3612

Cited by 19 publications

(9 citation statements)

References 27 publications

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“…The identified candidate miRNA was miR-101, which is linked to frizzled-4, F-box/WD repeat containing protein 11 and ubiquitin-conjugating enzyme E2 A. Previous studies have reported that miR-101 is associated with various tumor types and may regulate chemotherapeutic sensitivity in acute lymphoblastic leukemia ( 46 , 47 ). However, there have been no studies focusing on the association between miR-101 and NAFLD, to the best of our knowledge.…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes in non‑alcoholic fatty liver disease progression based on bioinformatics analysis

Liu

et al. 2018

Mol Med Report

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Due to economic development and lifestyle changes, the incidence of non-alcoholic fatty liver disease (NAFLD) has gradually increased in recent years. However, the pathogenesis of NAFLD is not yet fully understood. To identify candidate genes that contribute to the development and progression of NAFLD, two microarray datasets were downloaded from the Gene Expression Omnibus database. The differentially expressed genes (DEGs) were identified and functional enrichment analyses were performed. A protein-protein interaction network was constructed and modules were extracted using the Search Tool for the Retrieval of Interacting Genes and Cytoscape. The enriched functions and pathways of the DEGs included ‘cellular macromolecule biosynthetic process’, ‘cellular response to chemical stimulus’, ‘extracellular matrix organization’, ‘metabolic pathways’, ‘insulin resistance’ and ‘forkhead box protein O1 signaling pathway’. The DEGs, including type-1 angiotensin II receptor, formin-binding protein 1-like, RNA-binding protein with serine-rich domain 1, Ras-related C3 botulinum toxin substrate 1 and polyubiquitin-C, were identified using multiple bioinformatics methods and validated in vitro with reverse transcription-quantitative polymerase chain reaction analysis. In conclusion, five hub genes were identified in the present study, and they may aid in understanding of the molecular mechanisms underlying the development and progression of NAFLD.

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Section: Discussionmentioning

confidence: 99%

Identification of key genes in non‑alcoholic fatty liver disease progression based on bioinformatics analysis

Liu

et al. 2018

Mol Med Report

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“…Later, studies further confirm that miR-101-3p targets EZH2 and suppresses proliferation and migration of PCa cells [12,13]. After thoroughly reviewing published literature on PCa, we found that ten target genes including SOD1 [14], SUB1 [15], TIGAR [16], NR2F2 [17], RLIP76 [9], COX-2 [18], Glyoxalase 1 [19], ZEB1 [20], Slug [20] as well as EZH2 [11,13,21,22] were truly inhibited by miR-101-3p in PCa tissues or cells. Furthermore, we found that the target genes of miR-101-3p were enriched in many biological processes, such as positive regulation of transcription, intracellular signal transduction, protein autophosphorylation, activation of MAPKK activity.…”

Section: Discussionmentioning

confidence: 54%

Identification of potential targets of microRNA-101-3p in prostate cancer by bioinformatics analysis

Zhang¹,

Wang²,

Bai³

et al. 2019

Preprint

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Background: MiR-101-3p, a tumor suppressor, has been implicated as a tumor suppressor miRNA in multiple primary malignancies including prostate cancer (PCa). This study aimed to explore target genes and relevant signaling pathways regulated by microRNA-101-3p (miR-101-3p) for further researches in PCa with bioinformatics analysis. Results: 565 target genes were appeared in all databases and enriched in positive regulation of transcription, which were mainly enriched in axon guidance and MAPK pathway. Two important modules were detected from PPI network. Ten hub genes were selected, including MAPK1, PIKFYVE, EGFR, SMARCA4, TOP2B, GSK3B, FOS, RAC1, BCL2 and TAF1. After thoroughly reviewing published literature, we found that 10 target genes and six signaling pathways were truly inhibited by miR-101-3p in various tissues or cells; some of these verified targets were in accordance with our present prediction. Conclusion: This study demonstrated that miR-101-3p target hub genes, including MAPK1, PIKFYVE, EGFR, SMARCA4, TOP2B, GSK3B, FOS, RAC1, BCL2 and TAF1, might promote the development of PCa. However, further experiments are still required to confirm potential functions of these miR-101-3p target genes and pathways in PCa.

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“…Among these drug-related miRNAs, miR-101 is usually downregulated in cancers. Furthermore, miR-101 is found to sensitize gastric cancer, prostate cancer, bladder cancer and hepatocellular carcinoma cells to anti-tumor drugs [ 27 , 28 , 29 , 30 ]. These reports demonstrate that miR-101 is a potential sensitizer for anti-tumor treatment.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of miR-101 promotes TRAIL-induced mitochondrial apoptosis in papillary thyroid carcinoma by targeting c-met and MCL-1

Zhu

2017

Oncotarget

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Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) induces apoptosis in malignant cells, but not in normal cells. As papillary thyroid carcinoma cells broadly expressed TRAIL receptors (death receptor 4 and death receptor 5) on their surface, TRAIL is considered as a promising drug for treatment of papillary thyroid carcinoma. However, resistance to TRAIL still be a big obstacle to achieve a satisfactory effect for cancer therapy. Here, we found that overexpression of miR-101 was able to sensitize papillary thyroid carcinoma cells to TRAIL treatment in vitro and in vivo. Mechanically, we found that genes of c-met and MCL-1 were the targets of miR-101. Overexpression of miR-101 in TPC-1 significantly decreased the cellular protein levels of c-met and MCL-1, and thus inhibiting the PI3K/AKT pathway and reducing the resistance to TRAIL-induced mitochondrial apoptosis. Enforced expression of either c-met or MCL-1 could partially inhibit the miR-101 promoted apoptosis in TRAIL-treated TPC-1 cells. These results indicated that miR-101-c-met/MCL-1 axis determined the sensitivity of TRAIL to thyroid cancer in some extent. Combination with TRAIL and miR-101 may represent a novel approach to kill papillary thyroid carcinoma cells efficiently.

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miR-101 Enhances Cisplatin-Induced DNA Damage Through Decreasing Nicotinamide Adenine Dinucleotide Phosphate Levels by Directly Repressing Tp53-Induced Glycolysis and Apoptosis Regulator Expression in Prostate Cancer Cells

Cited by 19 publications

References 27 publications

Identification of key genes in non‑alcoholic fatty liver disease progression based on bioinformatics analysis

Identification of key genes in non‑alcoholic fatty liver disease progression based on bioinformatics analysis

Identification of potential targets of microRNA-101-3p in prostate cancer by bioinformatics analysis

Overexpression of miR-101 promotes TRAIL-induced mitochondrial apoptosis in papillary thyroid carcinoma by targeting c-met and MCL-1

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