Abstract
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. 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. 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. DCST1-AS1 may downregulate miR-29b through methylation in GBM to promote cancer cell proliferation.
Highlights
Glioblastoma (GBM) is the most malignant form of brain cancer, owing to the high mortality rate
MiR-29b was downregulated in GBM and inversely correlated with the expression of DCST1-AS1
In GBM cells, DCST1AS1 overexpression led to the downregulation of miR-29b and the increased methylation level of miR-29b gene
Summary
Glioblastoma (GBM) is the most malignant form of brain cancer, owing to the high mortality rate. We in this study analyzed the role of DCST1-AS1 in glioblastoma (GBM). Glioblastoma (GBM), refers to glioblastoma multiforme, is the most malignant form of brain cancer[1]. GBM only affects about 3 per 100,000 adults per year[2]. In spite of the low incidence rate, GBM is considered as a major cause of cancer deaths, owing to the high mortality rate[3, 4]. It has been estimated that only 25% GBM patients can survive longer than 1 year after the initial diagnosis even after active treatment[3, 4]. Novel therapeutic approaches are needed to improve the survival of GBM patients. Molecular mechanism of GBM remains hardly known, which challenge the development of more effective therapy [5, 6]
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