Long non‑coding RNA MDC1‑AS inhibits human gastric cancer cell proliferation and metastasis through an MDC1‑dependent mechanism

Qin, Ying; Zhuang, Shutong; Wen, Jianfeng; Zheng, Kai

doi:10.3892/etm.2017.5370

Cited by 9 publications

(9 citation statements)

References 26 publications

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“…As detailed above, numerous studies have linked MDC1 to carcinogenesis. MDC1 has primarily been characterized as a tumor suppressor, with studies showing MDC1 loss in a variety of cancers across organ systems [35,36,[38][39][40][41][42][43]87]. The model proposed is that the increased genomic instability resulting from MDC1 loss allows the potential for malignant transformation.…”

Section: Discussionmentioning

confidence: 99%

“…This suggests a role for antisense RNA in coding gene regulation. MDC1-AS (antisense) is a lncRNA that has been shown to be down-regulated in gastric cancer, bladder cancer, and glioma [39,40,87]. It is transcribed on the antisense strand of the MDC1 transcript (Fig.…”

Section: Regulation Of Mdc1 Levels In Cancermentioning

confidence: 99%

“…The mechanism by which this occurs is unclear, although one study has found that antisense RNA may increase the stability of the sense mRNA counterpart, in the case of β-secretase expression in Alzheimer's [88]. These findings have been recapitulated in glioma and gastric cancer, finding lower levels of MDC1-AS and MDC1 itself in tumors compared with benign tissue [39,87]. Consistent with this, analysis of RNA-seq data of normal tissues from the Human Protein Atlas (HPA) indicates that expression of MDC1 mRNA strongly correlates with expression of MDC1-AS in normal tissues, with r=.992 and p<.0001 (Fig.…”

Section: Regulation Of Mdc1 Levels In Cancermentioning

confidence: 99%

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Roles for MDC1 in cancer development and treatment

et al. 2020

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Section: Discussionmentioning

confidence: 99%

Section: Regulation Of Mdc1 Levels In Cancermentioning

confidence: 99%

Section: Regulation Of Mdc1 Levels In Cancermentioning

confidence: 99%

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Roles for MDC1 in cancer development and treatment

et al. 2020

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“…22 MDC1-AS inhibited gastric tumorigenesis through an MDC1-dependent mechanism. 23 On the other hand, HOTAIR was found to be highly expressed in GC and associated with poor overall survival in GC patients, suggesting that HOTAIR might be a potentially useful independent prognostic biomarker for GC. 24 LINC00689 is a lncRNA located at chromosome 7q36.3.…”

Section: Discussionmentioning

confidence: 99%

<p>LncRNA LINC00689 Promotes the Progression of Gastric Cancer Through Upregulation of ADAM9 by Sponging miR-526b-3p</p>

Yin

Tian

Amin

et al. 2020

CMAR

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Introduction: Increasing studies have demonstrated that noncoding RNAs, including miRNAs and lncRNAs, have vital roles in mediating cancer progression. However, the expression features and biological functions of LINC00689 in gastric cancer (GC) remain largely unknown. This study was designed to investigate the functions of LINC00689, miR-526b-3p and ADAM9 as well as their interactions in GC. Methods: Real time PCR(RT-PCR) was used to detect the expression of LINC0068, miR-526b-3p and ADAM9 in both GC tissues or cell lines. Gain-and loss-of functions of assays were conducted to verify the role of LINC0068, miR-526b-3p and ADAM9 in GC development. Cell proliferation were determined by CCK8 assay and transwell assay and scratch wound-healing assay were used to test cell invasion and migration. Further, the relationships between LINC00689 and miR-526b-3p, miR-526b-3p and ADAM9 were predicted by bioinformatics analysis and then proved by Luciferase reporter assay and RNA Immunoprecipitation(RIP) assay. Results: We found that LINC00689 was upregulated in GC tissues and positively correlated with advanced tumor stage and tumor size, while miR-526b-3p was downregulated. Furthermore, gain-and loss-of-function experiments revealed that LINC00689 promoted the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) of GC cells, while miR-526b-3p had the opposite effects. The underlying mechanisms indicated that LINC00689 functioned as a competing endogenous RNA (ceRNA) by sponging miR-526b-3p in GC cells. Further investigations confirmed that ADAM9 was a direct target of miR-526b-3p and positively modulated the progression of GC. Conclusion: Our study suggests that LINC00689 functions as a novel oncogenic lncRNA in the development of GC by promoting ADAM9 expression through suppression of miR-526b-3p.

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“…Recently, the roles of lncRNAs in GC process have been elucidated in details. For example, MDC1‐AS can inhibit GC cell proliferation and metastasis through regulating MDC1 . MACC1‐AS1 promotes GC cell metabolic plasticity through modulating AMPK, Lin28, and MACC1 .…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA DINO (damage induced noncoding) represses the development of gastric cancer by modulating p21 and Bcl‐2 Associated X Protein (Bax) expression

Yan

Cai²,

et al. 2019

J of Cellular Biochemistry

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lncRNAs are responsible for a variety of diseases, including gastric cancer (GC). Many recent studies have reported that lncRNAs can serve as crucial regulators of various genes. Nevertheless, the biological function of lncRNA damage induced noncoding (DINO) remained poorly investigated in GC. Therefore, in our present study, the detailed role of DINO was investigated. It was manifested that DINO was significantly downregulated in GC tissues. Then, DINO was modulated by infecting LV-DINO or by LV-shRNA in BGC-823 and MGC-803 cells. Moreover, it was displayed that GC cell proliferation was suppressed by DINO overexpression, whereas silencing DINO increased cell proliferation significantly. For another, it was indicated that DINO dramatically induced apoptotic ratios of BGC-823 and MGC-803 cells, whereas the decrease of DINO depressed GC cell apoptosis. Apart from these, GC cell cycle progression was greatly blocked by LV-DINO. Furthermore, Western blot results displayed that upregulation of DINO elevated p21 expression and Bax expression. Oppositely, inhibition of DINO greatly suppressed p21 and Bax protein expression level. Taken these, DINO might exert a tumor inhibitory role in the progression of GC through modulating p21 and Bax. K E Y W O R D SBax, damage induced noncoding (DINO), gastric cancer (GC), p21 Recently, the roles of lncRNAs in GC process have been elucidated in details. For example, MDC1-AS can inhibit GC cell proliferation and metastasis through regulating MDC1. 9 MACC1-AS1 promotes GC cell metabolic plasticity through modulating AMPK, Lin28, and MACC1. 10 Besides, CASC15 can regulate GC cell proliferation, migration, and J Cell Biochem. 2019;120:11190-11195. wileyonlinelibrary.com/journal/jcb 11190 |

show abstract

Long non‑coding RNA MDC1‑AS inhibits human gastric cancer cell proliferation and metastasis through an MDC1‑dependent mechanism

Cited by 9 publications

References 26 publications

Roles for MDC1 in cancer development and treatment

Roles for MDC1 in cancer development and treatment

<p>LncRNA LINC00689 Promotes the Progression of Gastric Cancer Through Upregulation of ADAM9 by Sponging miR-526b-3p</p>

Long noncoding RNA DINO (damage induced noncoding) represses the development of gastric cancer by modulating p21 and Bcl‐2 Associated X Protein (Bax) expression

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