Characterization of selective exosomal microRNA expression profile derived from laryngeal squamous cell carcinoma detected by next generation sequencing

Huang, Qiang; Yang, Jin; Zheng, Jie; Hsueh, Chi‐Yao; Guo, Yang; Zhou, Liang

doi:10.3892/or.2018.6672

Cited by 43 publications

(53 citation statements)

References 38 publications

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“…Coincidentally, Yamada et al found that colorectal cancer cell‐derived microvesicles comprising microRNA‐1246 stimulate angiogenesis by stimulating Smad 1/5/8 signaling prompted by PML downregulation in endothelial cells . We established that miR‐1246 is extremely augmented in sEV acquired from LSCC cell lines in previous research; however, in‐depth research about its specific mechanism was absent …”

Section: Introductionmentioning

confidence: 72%

Lack of miR‐1246 in small extracellular vesicle blunts tumorigenesis of laryngeal carcinoma cells by regulating Cyclin G2

et al. 2020

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Small extracellular vesicle (sEV) has precise impacts on tumor microenvironment and play vital functions in intercellular interaction. However, the functional role of sEV miRNA on laryngeal squamous cell carcinoma (LSCC) is largely unresolved. Here, the expression of miR‐1246 in LSCC tissues and plasma sEV was examined. The internalization ability of sEV was determined by uptake assay. Then, the source and purity of sEV were checked through RNase and/or pharmacological inhibitors application. The invasion, migration, proliferation, and cell cycle assays were used to determine the altered abilities of miR‐1246 in sEV in LSCC. Finally, target gene of miR‐1246, Cyclin G2 (CCNG2), was stained immunohistochemically. In addition, the relationship between CCNG2 and clinicopathological features of patients was analyzed. We found that miR‐1246 was higher in LSCC tissues and plasma sEV. MiR‐1246 was enriched in sEV rather than soluble form. SEV could be internalized into adjacent cells. Lack of miR‐1246 in sEV abrogated the tumorigenesis of LSCC. Furthermore, CCNG2 knockdown arrested the cell cycle and correlated to clinicopathological features and prognosis of LSCC patients. Taken together, we found that the function of sEV miR‐1246 by regulating CCNG2 is responsible for LSCC advancement with emphasis on the main source of miR‐1246 mainly root in sEV rather than in soluble form.

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Section: Introductionmentioning

confidence: 72%

Lack of miR‐1246 in small extracellular vesicle blunts tumorigenesis of laryngeal carcinoma cells by regulating Cyclin G2

et al. 2020

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“…Exosomes are extracellular vesicles (30-100 nm), that acts as cargo for mRNAs, miRNAs, DNA fragments, proteins as well as apoptotic bodies [7]. Expression pattern of exosomal-derived miRNAs differ greatly between cancer and normal control cells [8,9], thereby hinting at the role of exosomal miRNAs as potential biomarker for cancer diagnosis, including OSCC. Several pioneering studies highlight the crucial role of exosomes in facilitating tumor growth, angiogenesis, invasion, metastasis as well as in conferring chemoresistance [10,11].…”

Section: Research Papermentioning

confidence: 99%

Exosome mediated miR-155 delivery confers cisplatin chemoresistance in oral cancer cells via epithelial-mesenchymal transition

et al. 2020

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Cisplatin is used as chemotherapeutic drug for oral squamous cell carcinoma (OSCC). However, OSCC cells develop resistance following long-term cisplatin exposure. Resistance against cisplatin chemo-therapy is accredited to the process of epithelial-to-mesenchymal transition, which in-turn has been linked to tumorrecurrence. miRNA deregulation, a common event in cancer, plays contributory role in chemo-resistance. Exosomes acts as the natural cargo for miRNA and facilitates inter-cell communication in the tumor micro-environment. Hence, exosomal-mediated miRNA transference may play essential role in drug resistance and serve as a target for cancer-therapy. miR-155 upregulation in OSCC has been described, however, its relevance in the observed chemo-resistance is unclear and also, if exosomes have any role in miR-155 regulation remain elusive. In the present study, we document for the first time the critical role of exosomes in mediating increments in miR-155 expression in OSCC cells that have acquired cisplatin resistance (cis Res cells). Importantly, exosomal transfer from cis Res to the cisplatin sensitive (cis Sens) cells was found to confer significant miR-155 induction in the recipient cis Sens cells. Restoration of miR-155 expression in cis Sens cells following miR-155 mimics treatment led to epithelial to mesenchymal transition, enhancements in their migratory potential as well as acquisition of resistant phenotype. Notably, similar augmentations in the migratory and chemo-resistant traits were seen upon delivery of exosomes from cis Res to the recipient cis Sens cells. Overall, our findings establish the significance of exosomalmediated miR-155 shuttling in the cisplatin-chemoresistance, commonly observed in OSCC cells, thereby providing rationale for targeting miR-155 signalling for oral cancer therapy.

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“…The resulting exosome supernatant was then ltered (0.22 μm lter) to eliminate cellular debris, followed by centrifugal ultra ltration (Amicon® Ultra-15 100 KDa; Merck KGaA) to prevent potential contamination. Exosomes were isolated from the ultra ltered supernatant with Ribo™ Exosome Isolation Reagent (RiboBio Co., Ltd., Guangzhou, China), as previously described [13]. Brie y, the collected conditioned medium was mixed with Ribo™ Exosome Isolation Reagent (ratio 3:1), followed by an incubation at 4˚C overnight.…”

Section: Collection Of Culture Supernatant and Isolation Of Exosomesmentioning

confidence: 99%

“…Transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA) TEM was used to identify the morphological characteristics of exosome pellets, as described previously [13]. About 20 μL of exosome-PBS solution was added to carbon-coated copper grids for 1 min and then the excess solution was removed by blotting with lter paper.…”

Section: Collection Of Culture Supernatant and Isolation Of Exosomesmentioning

confidence: 99%

“…The sRNA next-generation sequencing technology was used to investigate differences in the miRNA pro les between exosomes from the three pairs of CAFs and NFs. The sRNA library preparation and sample sequencing were performed with the assistance of RiboBio Co., Ltd. (Guangzhou, China) using an Illumina HiSeq™ 2500 device, as described previously [13]. Brie y, total RNA from the three pairs of CAF and NF exosomes were concatenated with 5'-and 3'-adaptors, followed by cDNA synthesis and PCR ampli cation.…”

Section: Extraction Of Total Rnamentioning

confidence: 99%

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Aberrant expression profiles and bioinformatic analysis of CAF-derived exosomal miRNAs from three moderately differentiated supraglottic LSCC patients

Wang

Huang

et al. 2020

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Background Aberrant expression of exosomal miRNAs has emerged as a research hotspot in cancer studies. However, no studies have been conducted on the dysregulation of exosomal miRNAs derived from cancer-associated fibroblasts (CAFs) in supraglottic laryngeal squamous cell carcinoma (SLSCC). Methods CAFs and paired normal fibroblasts (NFs) from SLSCC patients were cultured, and exosomes in the culture supernatants were collected and identified by transmission electron microscopy, nanoparticle tracking analysis and western blotting. Exosomal miRNA expression was compared in each pair of CAFs and NFs by next-generation sequencing. Four online bioinformatic algorithms predicted the potential target genes of aberrantly expressed miRNAs, while gene ontology and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment and network analysis identified downstream target genes and their interactions. Results Three pairs of CAFs and NFs were successfully cultured and purified. CAF-derived exosomal miRNAs were mostly downregulated and included miR-656-3p, miR-337-5p, miR-29a-3p and miR-655-3p; however, some, including miR-184-3p, miR-92a-1-5p, miR-212-3p and miR-3135b, were upregulated. Bioinformatics analysis revealed involvement of these miRNAs in biological processes, cellular components and molecular functions. KEGG analysis revealed the top thirty pathways involvement in cancer initiation and progression and in cell cycle regulation. An interaction network showed miR-16-5p, miR-29a-3p, miR-34c-5p, miR-32-5p and miR-490-5p as the top five miRNAs and CCND1, CDKN1B, CDK6, PTEN and FOS as the top five target genes. Conclusions SLSCC patients showed aberrant expression of CAF-derived exosomal miRNAs. The target genes may jointly constitute a carcinogenic tumour microenvironment and may play decisive roles in the initiation and progression of SLSCC.

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Characterization of selective exosomal microRNA expression profile derived from laryngeal squamous cell carcinoma detected by next generation sequencing

Cited by 43 publications

References 38 publications

Lack of miR‐1246 in small extracellular vesicle blunts tumorigenesis of laryngeal carcinoma cells by regulating Cyclin G2

Lack of miR‐1246 in small extracellular vesicle blunts tumorigenesis of laryngeal carcinoma cells by regulating Cyclin G2

Exosome mediated miR-155 delivery confers cisplatin chemoresistance in oral cancer cells via epithelial-mesenchymal transition

Aberrant expression profiles and bioinformatic analysis of CAF-derived exosomal miRNAs from three moderately differentiated supraglottic LSCC patients

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