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LncRNA DSCAM-AS1 facilitates the progression of endometrial cancer via miR-136-5p.

ABSTRACT: Previous studies have indicated that long non-coding RNA (lncRNA) down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) serves an oncogenic role in numerous cancer types. However, its role in endometrial cancer (EC) remains largely unknown. In the present study, DSCAM-AS1 expression levels in EC tissues and cells and their normal counterparts were analyzed using reverse transcription-quantitative. In vitro and in vivo experiments were conducted to validate the functions of DSCAM-AS1 in EC. It was revealed that DSCAM-AS1 was expressed at a high level in EC tissues and cells after analyzing patient data and data obtained from The Cancer Genome Atlas. Notably, it was also revealed that high DSCAM-AS1 expression was associated with a less favorable overall survival in patients with EC. Knockdown of DSCAM-AS1 was able to suppress EC cell proliferation by upregulating cell apoptosis in vitro. Furthermore, it was revealed that DSCAM-AS1 acted as a microRNA (miR)-136-5p sponge to exert its oncogenic roles in EC. Collectively and to the best of our knowledge, the current results provided first evidence that DSCAM-AS1 stimulated EC progression by regulating miR-136-5p, which may improve the understanding of the roles of ncRNAs in EC, and may help identify novel targets for anticancer treatment.

SUBMITTER: Li L

PROVIDER: S-EPMC8527824 | biostudies-literature | 2021 Dec

REPOSITORIES: biostudies-literature

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lncRNA DSCAM-AS1 facilitates the progression of endometrial cancer via miR-136-5p.

Li Luhong L Chen Peipei P Huang Bingbing B Cai Peiya P

Oncology letters 20211012 6

Previous studies have indicated that long non-coding RNA (lncRNA) down syndrome cell adhesion molecule antisense 1 (DSCAM-AS1) serves an oncogenic role in numerous cancer types. However, its role in endometrial cancer (EC) remains largely unknown. In the present study, DSCAM-AS1 expression levels in EC tissues and cells and their normal counterparts were analyzed using reverse transcription-quantitative. <i>In vitro</i> and <i>in vivo</i> experiments were conducted to validate the functions of D ...[more]

PMID: 34691252

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Project description:BackgroundBreast cancer (BC) is a prevalent malignancy with complex etiology and varied clinical behavior. Long non-coding RNAs (lncRNAs) have emerged as key regulators in cancer progression, including BC. Among these, lncRNA TDRKH-AS1 has been implicated in several cancers, but its role in BC remains unclear.MethodsWe conducted a comprehensive investigation to elucidate the role of TDRKH-AS1 in BC. Clinical samples were collected from BC patients, and BC cell lines were cultured. Bioinformatics analysis using the starBase database was carried out to assess TDRKH-AS1 expression levels in BC tissue samples. Functional experiments, including knockdown, colony formation, CCK-8, Transwell, and wound-healing assays, were conducted to determine the role of TDRKH-AS1 in BC cell proliferation and invasion. Luciferase reporter and RIP assays were used to examine the interactions between TDRKH-AS1 and miR-134-5p. In addition, the downstream target gene of miR-134-5p, cAMP response element-binding protein 1 (CREB1), was identified and studied using various methods, including RT-qPCR, immunoprecipitation, and rescue experiments. In vivo experiments using mouse tumor xenograft models were conducted to examine the role of TDRKH-AS1 in BC tumorigenesis.ResultsTDRKH-AS1 was found to be significantly upregulated in BC tissues and cell lines. High TDRKH-AS1 expression correlated with advanced BC stages and worse patient outcomes. Knockdown of TDRKH-AS1 led to decreased BC cell proliferation and invasion. Mechanistically, TDRKH-AS1 acted as a sponge for miR-134-5p, thereby reducing the inhibitory effects of miR-134-5p on CREB1 expression. Overexpression of CREB1 partially rescued the effects of TDRKH-AS1 knockdown in BC cells. In vivo studies further confirmed the tumor-promoting role of TDRKH-AS1 in BC.ConclusionsOur study unveiled a novel regulatory axis involving TDRKH-AS1, miR-134-5p, and CREB1 in BC progression. TDRKH-AS1 functioned as an oncogenic lncRNA by promoting BC cell proliferation and invasion through modulation of the miR-134-5p/CREB1 axis. These findings highlighted TDRKH-AS1 as a potential diagnostic biomarker and therapeutic target for BC treatment.

Dataset Information

LncRNA DSCAM-AS1 facilitates the progression of endometrial cancer via miR-136-5p.

Publications

lncRNA DSCAM-AS1 facilitates the progression of endometrial cancer via miR-136-5p.

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