miR-486-5p inhibits cell growth of papillary thyroid carcinoma by targeting fibrillin-1

Ma, Xinfeng; Wei, Jing; Zhang, Li; Deng, Deqiang; Liu, Lianyong; Xin, Mei; He, Xiaohua; Tian, Jia-Sheng

doi:10.1016/j.biopha.2016.03.020

Cited by 45 publications

(40 citation statements)

References 28 publications

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“…Also, the depleted SNHG12 upregulated miR-195-5p to downregulate Notch2, thus suppressing the progression of osteosarcoma [32]. Moreover, Ma et al revealed that FBN1 was a target gene of miR-486-5p, whereby the elevated expression of miR-486-5p could target FBN1 to suppress the development of papillary thyroid carcinoma [33]. It was revealed that miR-140-5p negatively regulated IP3k2 to suppress autophagy in osteosarcoma after chemotherapy [11].…”

Section: Discussionmentioning

confidence: 99%

Long non-coding RNA PGM5-AS1 modulates epithelial-mesenchymal transition and invasion and metastasis of osteosarcoma cells by impairing miR-140-5p-mediated FBN1 inhibition

Liu

Gao

et al. 2019

Preprint

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Background Osteosarcoma represents a uncommon tumor occurring in bone possessing elevated rate of incidence and reduced rate of healing. Hence, developing effective therapeutic modalities to treat osteosarcoma is essential. Various long non-coding RNAs (lncRNAs) are engaged in prognostic and diagnostic processes of diseases. Thus, we identified the molecular mechanism of lncRNA PGM5-AS1 in progression of osteosarcoma.Methods Microarray-based analysis was employed to screen the osteosarcoma-related differentially expressed lncRNA. PGM5-AS1 level in osteosarcoma tissues and cells as well as the levels of microRNA-140-5p (miR-140-5p) and fibrillin-1 (FBN1) in osteosarcoma tissues were determined. Dual-luciferase reporter gene assay, RNA pull-down assay, and RNA immunoprecipitation assay were done to find out the relation among PGM5-AS1, miR-140-5p, and FBN1. shRNA, mimic, or inhibitor was applied to alter the levels of PGM5-AS1, miR-140-5p, and FBN1 in osteosarcoma cells to investigate how they regulated migration, invasion, and epithelial-mesenchymal transition (EMT) of osteosarcoma cells in vitro. The nude mice were injected with osteosarcoma cell line with depleted PGM5-AS1 to detect the role of PGM5-AS1 in tumorigenesis in vivo.Results PGM5-AS1 possessing elevated level in osteosarcoma was identified as the differentially expressed lncRNA in osteosarcoma. Osteosarcoma tissues exhibited low miR-140-5p expression and high FBN1 expression. Results confirmed that PGM5-AS competitively bound to miR-140-5p to upregulate FBN1. Also, hindering PGM5-AS1 and FBN1 or enforcing miR-140-5p dampened migration, invasion, and EMT of osteosarcoma cells in vitro. Furthermore, silencing PGM5-AS1 markedly inhibited tumorigenesis in vivo.Conclusion All in all, PGM5-AS1 depletion causes FBN1 reduction to retard osteosarcoma processes by negatively modulating miR-140-5p, highlighting PGM5-AS1 silencing as a biomarker for osteosarcoma management.

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Section: Discussionmentioning

confidence: 99%

Long non-coding RNA PGM5-AS1 modulates epithelial-mesenchymal transition and invasion and metastasis of osteosarcoma cells by impairing miR-140-5p-mediated FBN1 inhibition

Liu

Gao

et al. 2019

Preprint

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“…miR-486-5p is downregulated in CRC tissues compared with the adjacent non-tumor tissues and the CRC mice mode presents increased miR-486-5p suppresses tumor growth and lymphangiogenesis (21). miR-486-5p is significantly downregulated in PCT tissues and cell lines and its underexpression promotes cell proliferation and represses cell apoptosis in PTC (22). It is reported that miR-486-5p is downregulated in lung adenocarcinoma and COL4A2 is upregulated in non-small cell lung cancer and small cell lung cancer (23,25).…”

Section: Discussionmentioning

confidence: 99%

“…These protein-coding genes were significantly up-regulated in LSCC and enriched in 12 signaling pathways (Table V), covering focal adhesion, ECM-receptor interaction, mTOR signaling pathway and cytokine-cytokine receptor interaction. miR-486 functions as a tumor suppressor in several types of tumor covering colorectal cancer (CRC), papillary thyroid carcinoma (PCT) and lung cancer (21)(22)(23). miR-486-5p is downregulated in laryngeal carcinoma by microarray (24) and the roles of miR-486-5p in LSCC are unclear.…”

Section: Discussionmentioning

confidence: 99%

Identification of miRNA-mRNA crosstalk in laryngeal squamous cell carcinoma

Fei

Guo

Wang³

et al. 2017

Molecular Medicine Reports

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The aim of the present study was to elaborate the underlying pathogenesis of laryngeal squamous cell carcinoma (LSCC). Micro (mi) RNA and messenger (m) RNA expression profiling of patients with LSCC were downloaded from The Cancer Genome Atlas (TCGA) database. Differentially expressed miRNAs (DEMIs) and differentially expressed mRNAs (DEMs) were identified in LSCC compared to normal control tissues. The DEMs targeted by DEMIs were identified and the negative correlation between DEMs and DEMIs was subjected to visualization. The potential functions of DEMs targeted by DEMIs were annotated in Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) database. A total of 663 dysregulated DEMs (449 upregulated and 214 downregulated) and 33 DEMIs (24 upregulated and 8 downregulated) were identified in LSCC compared with normal controls. 502 negative correlations between DEMIs and DEMs were identified and subjected to construct interaction network. In the network, hsa‑miR‑486, ‑34c, ‑206 and ‑182 had the highest connectivity with DEMs, and respectively regulated 39, 33, 28 and 27 DEMs. DEMs targeted by DEMIs were significantly enriched in signal transduction, actin binding and extracellular region of GO terms and focal adhesion and extracellular matrix‑receptor interaction of KEGG pathways. The present study may provide valuable information for understanding the potential oncogenesis mechanism in LSCC and provide the foundation work for diagnosis biomarkers and therapeutic targets for LSCC.

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“…FBN1 was identified as a direct target of miR-486-5p in PTC cells [143]. FBN1 is upregulated PTC and implicated in cell growth, motility, and epithelial-mesenchymal transition [143,144].…”

Section: Micrornas In Differentiated Thyroid Cancermentioning

confidence: 99%

Multi-omics Signatures and Translational Potential to Improve Thyroid Cancer Patient Outcome

Boufraqech

Nilubol

2019

Cancers

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Recent advances in high-throughput molecular and multi-omics technologies have improved our understanding of the molecular changes associated with thyroid cancer initiation and progression. The translation into clinical use based on molecular profiling of thyroid tumors has allowed a significant improvement in patient risk stratification and in the identification of targeted therapies, and thereby better personalized disease management and outcome. This review compiles the following: (1) the major molecular alterations of the genome, epigenome, transcriptome, proteome, and metabolome found in all subtypes of thyroid cancer, thus demonstrating the complexity of these tumors and (2) the great translational potential of multi-omics studies to improve patient outcome.

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miR-486-5p inhibits cell growth of papillary thyroid carcinoma by targeting fibrillin-1

Cited by 45 publications

References 28 publications

Long non-coding RNA PGM5-AS1 modulates epithelial-mesenchymal transition and invasion and metastasis of osteosarcoma cells by impairing miR-140-5p-mediated FBN1 inhibition

Long non-coding RNA PGM5-AS1 modulates epithelial-mesenchymal transition and invasion and metastasis of osteosarcoma cells by impairing miR-140-5p-mediated FBN1 inhibition

Identification of miRNA-mRNA crosstalk in laryngeal squamous cell carcinoma

Multi-omics Signatures and Translational Potential to Improve Thyroid Cancer Patient Outcome

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