LncRNA ADPGK-AS1 promotes pancreatic cancer progression through activating <i>ZEB1</i>-mediated epithelial–mesenchymal transition

Song, Shuxin; Yu, Weihua; Shi, Lin; Zhang, Mingbao; Wang, Teng; Guo, Shuang; Wang, Hongbo

doi:10.1080/15384047.2018.1423912

Cited by 27 publications

(15 citation statements)

References 34 publications

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“…A coexpression network revealed a hub comprising lncRNAs (MIR210HG, SNHG1, and LOC729970) and mRNAs (RAB3D, DDX17, and SPNS2) that presumably mediate drug resistance in pancreatic cancer [24]. This information might illustrate its function in tumor biology [25]. However, the role and mechanism of MIR210HG in IBC has not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

The long noncoding RNA MIR210HG promotes tumor metastasis by acting as a ceRNA of miR-1226-3p to regulate mucin-1c expression in invasive breast cancer

Zhou

Luo

et al. 2019

Aging

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Background: Long noncoding RNAs have been known to be involved in multiple types of malignancies, including invasive breast cancer (IBC). This study aimed to explore the role of long noncoding RNAs in IBC and elucidate the potential molecular mechanisms. Methods: Using TCGA microarray data analysis, we identified a long noncoding RNA, MIR210HG, highly expressed in IBC. Kaplan-Meier method and the log-rank test were used for survival analysis. The gain-of-function experiments were performed to assess the function of MIR210HG in IBC invasion and migration in both in vitro and in vivo settings. Bioinformatic analysis as well as luciferase reporter assay, rescue experiments and western blot assay revealed the mode of action of MIR210HG. Results: The aberrantly enhanced MiR210HG expression predicted poor prognosis and lower survival rate. Knockdown of MiR210HG suppressed IBC cell invasion and metastasis both in vitro and in vivo . MiR-1226-3p was identified and validated to be the target miRNA of MiR210HG. Furthermore, MiR210HG functions as a competing endogenous RNAs (ceRNA) which sponges miR-1226-3p, therefore upregulates the expression of mucin1 (MUC1-C). Conclusions: Our study demonstrated that MiR210HG sponges miR-1226-3p to facilitate invasive breast cancer cell invasion and metastasis by regulating mucin-1c and EMT pathway, revealing the oncogenic role of MiR210HG in IBC cells.

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Section: Discussionmentioning

confidence: 99%

The long noncoding RNA MIR210HG promotes tumor metastasis by acting as a ceRNA of miR-1226-3p to regulate mucin-1c expression in invasive breast cancer

Zhou

Luo

et al. 2019

Aging

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“…Zinc finger E-box binding homeobox 1 antisense 1 (ZEB1-AS1) is a long coding RNA which is an antisense transcript generated from ZEB1 promoters. Meanwhile, ZEB1-AS1 is overexpressed in many cancers such as bladder cancer [12], prostate cancer [13], gastric cancer [14], esophageal cancer [17], pancreatic cancer [18], osteosarcoma [19], and breast cancer [20]. In colorectal cancer, ZEB1-AS1 also plays an important role in the development and progression.…”

Section: Discussionmentioning

confidence: 99%

LncRNA ZEB1-AS1 regulates colorectal cancer cells by miR-205/YAP1 axis

Jin

Chen

2020

Open Medicine

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AbstractBackgroundRecent studies demonstrated that long non-coding RNAs (lncRNAs) were involved in many biological processes. Dysregulated lncRNAs are related to many cancers, including colorectal cancer (CRC). However, the molecular mechanism of lncRNA ZEB1-AS1 in CRC is not clear.MethodsLncRNA ZEB1-AS1, miR-205, and YAP1 expression were measured by quantitative reverse transcriptase PCR (QRT-PCR). YAP1 protein expression was measured by western blotting. Cell viability was measured by MTT assay. Cell apoptosis was detected by flow cytometry. Luciferase reporter assay was used to confirm the relationship between ZEB1-AS1, miR-205, and YAP1.ResultsLncRNA ZEB1-AS1 and YAP1 was upregulated in CRC tissues. The expression of YAP1 was positively correlated with ZEB1-AS1. Knockdown of ZEB1-AS1 inhibited cell viability and induced apoptosis in CRC cell line SW480 and HCT116 which could be reversed by overexpression of YAP1. ZEB1-AS1 targeted and regulated miR-205 which could directly bind to YAP1. Meanwhile, ZEB1-AS1 regulated the expression of YAP1 via modulating miR-205.ConclusionLong non-coding RNA ZEB1-AS1 silencing could inhibit cell proliferation and induce apoptosis of colorectal cancer via regulating miR-205 and YAP1.

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“…After washing, the sections were incubated with 50 μL of TUNEL at 37°C for 1 h. After mounting the sections with the anti-fade mounting medium, the fluorescence intensity was observed under a fluorescence microscope. The number of TUNEL-positive cells was counted under five randomly selected high-power fields ( Song et al, 2018 ).…”

Section: Methodsmentioning

confidence: 99%

Long Non-coding RNA MIAT Knockdown Prevents the Formation of Intracranial Aneurysm by Downregulating ENC1 via MYC

Zhao

Liu

et al. 2021

Front. Physiol.

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Intracranial aneurysm (IA) is vascular enlargement occurred on the wall of cerebral vessels and can result in fatal subarachnoid hemorrhage when ruptured. Recent studies have supported the important role of long non-coding RNAs (lncRNAs) in IA treatment. This study identified functional significance of lncRNA myocardial infarction associated transcript (MIAT) in IA. Myocardial infarction associated transcript and ectodermal-neural cortex 1 (ENC1) expression was detected by reverse transcription quantitative polymerase chain reaction. Cell counting kit 8 assay flow cytometry were conducted to detect cell viability and apoptosis of endothelial cells in IA. The interaction among MIAT, ENC1, and myelocytomatosis oncogene (MYC) was analyzed by RNA pull down, RNA immunoprecipitation assay, chromatin immunoprecipitation assay, and dual luciferase reporter assay. Intracranial aneurysm was induced by ligating the left carotid artery and the bilateral posterior branch of the renal artery in rats for studying the role of MIAT and ENC1 in vivo. Myocardial infarction associated transcript and ENC1 were upregulated in IA. Endothelial cells in IA presented a decreased cell viability and an increased apoptotic rate. Myocardial infarction associated transcript could regulate the expression of ENC1, and MYC could bind to the promoter region of ENC1. High expression of MIAT increased endothelial cell apoptosis and vascular endothelial injury, while MIAT knockdown was identified to reduce the risk of IA both in vitro and in vivo through regulating ENC1. To sum up, MIAT silencing is preventive for IA occurrence by decreasing the MYC-mediated ENC1 expression, which represents a novel therapeutic target for IA.

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LncRNA ADPGK-AS1 promotes pancreatic cancer progression through activating ZEB1-mediated epithelial–mesenchymal transition

Abstract: ADPGK-AS1 inhibited miR-205-5p and therefore promoted PC progression through activating ZEB1-induced EMT.

Cited by 27 publications

References 34 publications

The long noncoding RNA MIR210HG promotes tumor metastasis by acting as a ceRNA of miR-1226-3p to regulate mucin-1c expression in invasive breast cancer

The long noncoding RNA MIR210HG promotes tumor metastasis by acting as a ceRNA of miR-1226-3p to regulate mucin-1c expression in invasive breast cancer

LncRNA ZEB1-AS1 regulates colorectal cancer cells by miR-205/YAP1 axis

Long Non-coding RNA MIAT Knockdown Prevents the Formation of Intracranial Aneurysm by Downregulating ENC1 via MYC

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