Abstract
Introduction
The role of DCST1-AS1 has been investigated in several types of cancer, while the role of DCST1-AS1 in glioblastoma (GBM) is unclear. This study aimed to investigate the role of DCST1-AS1 in GBM.
Methods
GBM and paired non-tumor tissues were collected from 62 GBM patients. Expression levels of DCST1-AS1 and miR-29b in paired tissue samples were determined by RT-qPCR. The role of DCST1-AS1 in regulating the methylation of miR-29b was assessed by methylation-specific PCR (MSP). Cell proliferation was analyzed by cell proliferation assay.
Results
It was observed that the upregulation of DCST1-AS1 in GBM predicted poor survival. MiR-29b was downregulated in GBM and inversely correlated with the expression of DCST1-AS1. In GBM cells, overexpression of DCST1-AS1 resulted in the downregulation of miR-29b and the increased methylation level of miR-29b gene. Overexpression of DCST1-AS1 resulted in increased cell proliferation. Moreover, Overexpression of DCST1-AS1 significantly reversed the inhibitory effects of miR-29b on cancer cell proliferation.
Conclusion
DCST1-AS1 may downregulate miR-29b through methylation in GBM to promote cancer cell proliferation.
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Funding
The work was supported by the Department of Rehabilitation, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University.
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YZ supervised the whole study, data analysis, manuscript preparation; SH, YY and XH had data collection and analysis, manuscript preparation.
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Ethical approval was obtained from the Ethics Committee of the Second Hospital of Shandong University. All procedures performed in studies involving human participants were in accordance with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. All patients signed the informed consent.
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Informed consent was obtained from all individual participants included in the study.
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Hu, S., Yao, Y., Hu, X. et al. LncRNA DCST1-AS1 downregulates miR-29b through methylation in glioblastoma (GBM) to promote cancer cell proliferation. Clin Transl Oncol 22, 2230–2235 (2020). https://doi.org/10.1007/s12094-020-02363-1
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DOI: https://doi.org/10.1007/s12094-020-02363-1