Abstract
BackgroundGlioma 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.MethodsLong 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.ResultsMicroarray 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.ConclusionOur study suggested CSC-derived exo-SNHG16 promoted cancer progression by activating TLR7/MyD88/NFκB/c-Myc signaling pathway.
Highlights
Glioma is one of the most common central nervous system malignant tumors, accounting for 45~60% of adult intracranial tumors
High level of Long non-coding RNA (lncRNA) SNHG16 indicated a poor prognosis in glioma patients We first performed microassay analysis, and the data showed the differentially expressed lncRNAs in normal and cancer tissues (Fig. 1A)
SNHG16 was packaged into exosomes and derived from Cancer stem cells (CSCs) To determine the origin of SNHG16 in glioma, we isolated CSCs from glioma cancer tissue; immunofluorescence assay was performed to identify the markers CD105 and Nestin for CSCs (Fig. 2A)
Summary
Glioma is one of the most common central nervous system malignant tumors, accounting for 45~60% of adult intracranial tumors. Zhang et al Stem Cell Research & Therapy (2021) 12:349 regulation, transcription, and post-transcriptional regulation [5, 6] but is closely related to a variety of tumorigenesis and development [7]. Recent studies have found that lncRNA contributes to the development of glioma [8] and closely relates to patients' prognosis [9, 10]. Further studies have found that it may inhibit tumorigenesis and development by selectively activating downstream gene transcription after activating p53 [12]. MEG3 may play the role of the tumor suppressor gene in glioma. It has been reported that lncRNA SNHG16 acted as an oncogene to promote tumor development in breast cancer, gastric cancer and other cancers [13, 14]. The roles and mechanism of SNHG16 in glioma have not been thoroughly identified
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