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Search terms: exosomes OR "extracellular vesicles" OR microvesicles OR microparticles. Direct link to the PubMed search here.

Effect of Plasma-Derived Exosomes of Refractory/Relapsed or Responsive Patients with Diffuse Large B-Cell Lymphoma on Natural Killer Cells Functions.

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Effect of Plasma-Derived Exosomes of Refractory/Relapsed or Responsive Patients with Diffuse Large B-Cell Lymphoma on Natural Killer Cells Functions.

Cell J. 2020 Apr;22(1):40-54

Authors: Zare N, Haghjooy Javanmard SH, Mehrzad V, Eskandari N, Andalib AR

Abstract
Objective: The purpose of this study was to investigate effect of plasma-derived exosomes of refractory/relapsed or responsive diffuse large B-cell lymphoma (DLBCL) patients on natural killer (NK) cell functions.
Materials and Methods: In this cross-sectional and experimental study, NK cells were purified from responsive patients (n=10) or refractory/relapsed patients (n=12) and healthy donors (n=12). NK cells were treated with plasma-derived exosomes of responsive or refractory/relapsed patients. We examined the expression levels of hsa-miR-155-5p, hsalet- 7g-5p, INPP5D(SHIP-1) and SOCS-1 in NK cells quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Percentages of NK cells expressing CD69, NKG2D and CD16, NK cell cytotoxicity and NK cell proliferation (using flow-cytometry) as well as interferon-gamma (IFN-γ) level in the supernatant of NK cells using ELISA were also investigated.
Results: We observed an increased level of hsa-miR-155-5p and a decreased level of SOCS-1 in NK cells treated with exosomes compared to untreated NK cell in healthy donors and DLBCL patients. An increase in hsa-miR-155-5p level was associated with an increased level of IFN-γ in healthy donors. The decreased levels of hsa-let-7g-5p were observed in NK cells treated with exosomes in comparison with untreated NK cells in DLBCL patients (P<0.05). There was no significant difference in the percentage of CD69+ NK cells and NKG2D+ NK cells in the absence or presence of exosomes of DLBCL patients in each group. Furthermore, we observed significant reduction of NK cell proliferation in DLBCL patients and healthy donors in the presence of exosomes of refractory/relapsed patients (P<0.05). A significant decrease was observed in cytotoxicity of NK cell in patients with DLBCL treated with exosomes of responsive patients.
Conclusion: Our findings demonstrated adverse effect of plasma-derived exosomes of DLBCL patients on some functions of NK cell. It was also determined that low NK cell count might be associated with impaired response to R-CHOP and an increased recurrence risk of cancer.

PMID: 31606965 [PubMed]

Natural Host-Induced Gene Silencing Offers New Opportunities to Engineer Disease Resistance.

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Natural Host-Induced Gene Silencing Offers New Opportunities to Engineer Disease Resistance.

Trends Microbiol. 2019 Oct 09;:

Authors: Hou Y, Ma W

Abstract
RNA silencing is an essential gene-regulation mechanism in eukaryotic organisms. Guided by small RNAs (sRNAs) of 20-25 nt in length, RNA silencing broadly governs a wide range of biological processes. In addition to regulating endogenous gene expression and inhibiting viral infection, accumulating evidence suggests that sRNAs can also function as antimicrobial agents against nonviral pathogens and directly silence gene targets in invading pathogen cells. Here, we summarize current understanding of this host-induced gene silencing (HIGS) process as a defense mechanism during natural infection. Specific focuses will be on recent advancement in the sRNA executors of HIGS and their potential delivery mechanisms from the plant host to filamentous eukaryotic pathogens, including fungi and Phytophthora species. Implications of these new findings in the applications of HIGS as a tool for engineering disease resistance is discussed.

PMID: 31606358 [PubMed - as supplied by publisher]

Icotinib-resistant HCC827 cells produce exosomes with mRNA MET oncogenes and mediate the migration and invasion of NSCLC.

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Icotinib-resistant HCC827 cells produce exosomes with mRNA MET oncogenes and mediate the migration and invasion of NSCLC.

Respir Res. 2019 Oct 12;20(1):217

Authors: Yu Y, Abudula M, Li C, Chen Z, Zhang Y, Chen Y

Abstract
BACKGROUND: Icotinib has been widely used in patients with non-small cell lung cancer (NSCLC), and have significantly enhanced the overall survival rate of NSCLC patients. However, acquired drug resistance limits its clinical efficacy. Tumor cell-derived exosomes have been reported to participate in various biological processes, including tumor invasion, metastasis and drug resistance.
MATERIALS AND METHODS: In the present study, drug resistance was measured by MTT assay. Exosomes were extracted from the cell supernatant using ultracentrifugation and identified by exosomal marker. HCC827 cells were treated with exosomes derived from icotinib-resistant (IR) HCC827 to observe the invasion and migration of parent cells. The expression of exo-mRNA was analyzed by reverse transcription-quantitative polymerase chain reaction (RT-PCR). In addition, 10 exo-mRNAs detecting from the plasma and bronchoalveolar lavage fluid (BALF) of NSCLC patients with icotinib treatment were used to establish a new drug resistant-warning formula.
RESULTS: The oncogene MET into exosomes was identified from icotinib-resistant lung cancer cells, and this was also presented in exosomes in NSCLC patients diagnosed with cancer metastasis after icotinib treatment. The knockdown of MET in exosomes significantly decreased the ability of invasion and migration in HCC827 cells.
CONCLUSION: It was suggested that MET might be specifically package and transferred by exosomes to modify the invasion and migration ability of the surrounding icotinib-sensitive cells.

PMID: 31606039 [PubMed - in process]

 

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