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Published on: July 29, 2011
Exosomal SNHG16 secreted by CSCs promotes glioma development via TLR7
Ruijie Zhang1, Peng Li2, Heli Lv2
1Department of Neurology, Heze Hospital of Traditional Chinese Medicine, Heze, 274000, Shandong, China.
Background:
Glioma is one of the most common central nervous system malignant tumors, accounting for 45~60% of adult intracranial tumors. However, the clinical treatment of glioma is limited. It is of great significance to seek new therapeutic methods for glioma via gene therapy.
Methods:
Long non-coding RNA (lncRNA) SNHG16 expression level was measured by microarray and qRT-PCR assay; ISH was used to identify the location of SNHG16. Cancer stem cells (CSCs) were separated from glioma tissues and identified using immunofluorescence. Exosomes were isolated from CSCs and cancer cells and identified by TEM and western blot. MTT, wound healing, transwell, and colony formation assay were performed to explore the role of SNHG16 or si-SNHG16 from CSCs on progression of glioma cells. RIP was used to verify the interaction between SNHG16 and TLR7. The experiment of Xenograft used for exploring the function of SNHG16/ TLR7/MyD88/NFκB/c-Myc on growth on glioma in vivo.
Results:
Microarray assay showed long non-coding RNA (lncRNA) SNHG16 was upregulated in glioma. Followed qRT-PCR also showed an increase of SNHG16 in glioma tissues; high expression of SNHG16 indicated a poor prognosis in glioma patients. Interestingly, SNHG16 was packaged into exosomes and derived from CSCs. Functional analysis showed exo-SNHG16 secreted by CSCs promoted the progression of glioma cell lines SHG44 and U251. Furthermore, SNHG16 interacted with TLR7 and activated NFκB/c-Myc signaling in glioma cells. And the silencing of TLR7 inhibited the progression of SHG44 and U251 cells by exo-SNHG16 from CSCs. In vivo tumorigenesis experiments showed that exo-SNHG16 induced glioma progression by activating TLR7/MyD88/NFκB/c-Myc signaling.
Conclusion:
Our study suggested CSC-derived exo-SNHG16 promoted cancer progression by activating TLR7/MyD88/NFκB/c-Myc signaling pathway.
Insights
Cancer stem cell-derived exosomes carrying long non-coding RNA SNHG16 promote glioma progression. This occurs by activating the TLR7/MyD88/NFκB/c-Myc signaling pathway, offering potential therapeutic targets for glioma gene therapy.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Research
Background:
- Glioma is a common and aggressive central nervous system tumor with limited treatment options.
- Gene therapy presents a significant avenue for developing novel therapeutic strategies for glioma.
Purpose of the Study:
- To investigate the role of long non-coding RNA (lncRNA) SNHG16 in glioma progression.
- To explore the mechanism by which SNHG16, particularly when packaged in exosomes derived from cancer stem cells (CSCs), influences glioma growth and signaling pathways.
Main Methods:
- Quantification of SNHG16 expression in glioma tissues using microarray and qRT-PCR.
- Isolation and identification of exosomes from glioma CSCs and cancer cells.
- Functional assays (MTT, wound healing, Transwell, colony formation) to assess the impact of SNHG16 on glioma cell progression.
- Investigation of the interaction between SNHG16 and TLR7 using RIP assay.
- In vivo tumorigenesis experiments in xenograft models to evaluate the SNHG16/TLR7/MyD88/NFκB/c-Myc signaling axis.
Main Results:
- SNHG16 was found to be upregulated in glioma tissues and associated with poor prognosis.
- SNHG16 was identified within exosomes secreted by glioma CSCs.
- Exosomal SNHG16 (exo-SNHG16) promoted the progression of glioma cell lines.
- SNHG16 was shown to interact with TLR7, activating the NFκB/c-Myc signaling pathway.
- Silencing TLR7 or inhibiting exo-SNHG16 from CSCs attenuated glioma cell progression.
- In vivo studies confirmed that exo-SNHG16 promotes glioma growth via the TLR7/MyD88/NFκB/c-Myc pathway.
Conclusions:
- Glioma CSC-derived exosomes carrying SNHG16 promote tumor progression.
- The mechanism involves the activation of the TLR7/MyD88/NFκB/c-Myc signaling pathway.
- Targeting exo-SNHG16 or the TLR7 pathway represents a potential therapeutic strategy for glioma.
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