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LINC02308 promotes the progression of glioma through activating mTOR/AKT-signaling pathway by targeting miR-30e-3p/TM4SF1 axis

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Abstract

Background

Glioma is a common brain malignancy, and the purpose of this study is to investigate the function of LINC02308 in glioma.

Methods

The differentially expressed lncRNAs were screened by microarray. The expression of LINC02308 in glioma tissues and cells was evaluated. The interaction among LINC02308, miR-30e-3p, and TM4SF1 was determined. Cell proliferation and apoptosis were evaluated. The expression of mTOR/AKT-signaling and apoptosis-related markers was detected by Western blot. A xenograft tumor mouse model was constructed to investigate the roles of LINC02308.

Results

LINC02308 was significantly overexpressed in glioma, and a high LINC02308 level was correlated with a poor prognosis. LINC02308 silencing markedly inhibited proliferation and reduced apoptosis of glioma cells and also suppressed tumor growth in the xenograft tumor mouse model. Finally, we demonstrated that LINC02308 played its oncogenic role through binding to miR-30e-3p so as to relieve miR-30e-3p-induced suppression of TM4SF1.

Conclusions

LINC02308 promoted glioma tumorigenesis as a sponge of miR-30e-3p to upregulate TM4SF1 and activate AKT/mTOR pathway.

Hypothesis diagram illustrates the function and mechanism of LINC02308 in glioma. A schematic representation of the functional mechanism of LINC02308 in glioma.

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Data availability

The data that support the findings of this study are available on request from the corresponding author Yang Cao, Department of Clinical Laboratory, The First Hospital of Jilin University, No. 3302 Jilin Road, Erdao District, Changchun City, Jilin Province, 130021, P. R. China. E-mail: YangCaoChangchun@163.com. Some data are not publicly available due to the possibility of compromising the privacy of research participants.

References

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Code availability

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Funding

This work was supported by the Science and Technology Project of Health Commission of Sichuan Province (Grant No. 18PJ430) and the Field of Scientific Research Develop Project of North Sichuan Medical College in 2017 (Grant No. CBY17-A-YB39).

Author information

Authors and Affiliations

Authors

Contributions

Xianfeng Gao and Xiaoya Wang supervised the whole study, performed data analysis, and prepared the manuscript. Huaiqiang He and Yang Cao collected and analyzed data and prepared the manuscript.

Corresponding author

Correspondence to Yang Cao.

Ethics declarations

Ethical approval and consent to participate

Informed consent was obtained from all individual participants included in the study. All procedures were approved by the Human and Animal Ethics Committee of Clinical Laboratory, the First Hospital of Jilin University.

Consent for publication

Not applicable.

Conflict of interest

All other authors have no conflicts of interest. We declare that we do not have any commercial or associative interest that represents a conflict of interest in connection with the work submitted.

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Supplementary Information

ESM 1

LINC02308 was upregulated in glioma tissues and predicted a poor prognosis in TCGA dataset. (A) The volcano plots of differentially expressed mRNAs in GSE103227 (fold change >1.0 and P < 0.05). The red points represent dysregulated lncRNAs, and blue points represent dysregulated mRNAs. (B) The expression of LINC02308 in glioma with different grades including glioblastoma (GBM) and low-grade glioma (LGG) in TCGA dataset was analyzed by GEPIA. (C) Survival analysis of glioma patients (overall survival and disease free survival) with high and low LINC02308 expression was performed by Kaplan-Meier curve in TCGA dataset. * P < 0.05 (PNG 671 kb)

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Gao, X., Wang, X., He, H. et al. LINC02308 promotes the progression of glioma through activating mTOR/AKT-signaling pathway by targeting miR-30e-3p/TM4SF1 axis. Cell Biol Toxicol 38, 223–236 (2022). https://doi.org/10.1007/s10565-021-09604-1

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  • DOI: https://doi.org/10.1007/s10565-021-09604-1

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