LncRNA DCST1-AS1 downregulates miR-29b through methylation in glioblastoma (GBM) to promote cancer cell proliferation
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RESEARCH ARTICLE
LncRNA DCST1‑AS1 downregulates miR‑29b through methylation in glioblastoma (GBM) to promote cancer cell proliferation S. Hu1 · Y. Yao1 · X. Hu1 · Y. Zhu2 Received: 5 March 2020 / Accepted: 28 April 2020 © Federación de Sociedades Españolas de Oncología (FESEO) 2020
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. Keywords Glioblastoma · DCST1-AS1 · miR-29b · Methylation
Introduction Glioblastoma (GBM), also 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, the high mortality rate of GBM makes it a major cause of cancer deaths [3, 4]. It has been estimated that only 25% GBM patients can survive for longer than 1 year after the initial diagnosis even after active treatment [3, 4]. Therefore, novel therapeutic approaches are needed to improve the survival of GBM patients. However,
* Y. Zhu [email protected] 1
Department of NeurosurgeryHuangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, Huangshi City 435000, Hubei Province, People’s Republic of China
Department of Rehabilitation, Huangshi Central Hospital, Affiliated Hospital of Hubei Polytechnic University, No. 141 Tianjin Road, Huangshi Gang District, Huangshi City 435000, Hubei Province, People’s Republic of China
2
the unclear molecular mechanism of GBM limits the development of more effective therapy [5, 6]. The occurrence and development of GBM involve multiple signaling pathways [7, 8]. Importantly, increasing knowledge of the functions of molecular players in GBM provides novel targets for the development of targeted therapy, which aims to suppress cancer development by regulating the expression of cancer-related genes [9, 10]. Non-coding RNAs (ncRNAs), such as miRNAs and long (> 200 nt) ncRNAs (lncRNAs), have no protein-coding capacity but can regulate gen
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