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ETS1-activated SNHG10 exerts oncogenic functions in glioma via targeting miR-532-3p/FBXL19 axis
Lide Jin1, Shengquan Huang1, Congjin Guan2
1The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, No.157 Jinbi Road, Kunming, 650032, Yunnan, China.
Background:
In past few years, long non-coding RNAs (lncRNAs) have been reported to play regulatory roles during cancer progression. LncRNA SNHG10 has been explored in several sorts of cancers. However, its detailed role and mechanism are still not well understood in glioma.
Methods:
Expression levels of genes were evaluated by RT-qPCR. EdU, TUNEL, sphere formation, wound healing and transwell assays appraised the effect of SNHG10 on glioma cellular processes. The interaction between molecules was examined by ChIP, RIP, RNA pull down and luciferase reporter assays.
Results:
High level of SNHG10 was detected in glioma cells. Functional assay confirmed that SNHG10 promoted the proliferation, migration, invasion and stemness of glioma cells. Moreover, miR-532-3p was validated to bind with SNHG10 and expressed at a low level in glioma cells. Importantly, miR-532-3p exerted inhibitory functions in glioma. Furthermore, it was found that FBXL19 targeted by miR-532-3p facilitated cell growth and stemness in glioma, and that SNHG10 worked in glioma by increasing FBXL19 expression through sequestering miR-532-3p. More importantly, ETS1 promoted the transcription of SNHG10 and it mediated contribution to the malignant behaviors of glioma cells by SNHG10/miR-532-3p/FBXL19 signaling.
Conclusion:
SNHG10 was transcriptionally activated by ETS1 and played an oncogenic role in glioma by sponging miR-532-3p and up-regulating FBXL19.
Insights
Long non-coding RNA SNHG10 promotes glioma progression by activating FBXL19 through sponging miR-532-3p. This oncogenic role is transcriptionally regulated by ETS1, highlighting a novel therapeutic target for glioma.
Area of Science:
- Molecular Biology
- Oncology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are increasingly recognized for their regulatory roles in cancer progression.
- LncRNA SNHG10 has been implicated in various cancers, but its specific function and mechanism in glioma remain unclear.
Purpose of the Study:
- To elucidate the role and underlying mechanism of lncRNA SNHG10 in glioma.
- To investigate the regulatory pathway involving SNHG10, miR-532-3p, and FBXL19 in glioma progression.
Main Methods:
- Gene expression analysis using RT-qPCR.
- Functional assays including EdU, TUNEL, sphere formation, wound healing, and Transwell assays.
- Molecular interaction studies employing ChIP, RIP, RNA pull-down, and luciferase reporter assays.
Main Results:
- SNHG10 expression is elevated in glioma cells and promotes proliferation, migration, invasion, and stemness.
- SNHG10 sponges miR-532-3p, which normally inhibits glioma cell growth and stemness by targeting FBXL19.
- ETS1 transcriptionally activates SNHG10, establishing the SNHG10/miR-532-3p/FBXL19 signaling axis in mediating glioma malignancy.
Conclusions:
- SNHG10 acts as an oncogene in glioma, driven by ETS1-mediated transcriptional activation.
- The SNHG10/miR-532-3p/FBXL19 pathway is crucial for glioma cell growth and stemness.
- Targeting this pathway presents a potential therapeutic strategy for glioma.
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