lncRNA XIST regulates proliferation and migration of hepatocellular carcinoma cells by acting as miR-497-5p molecular sponge and targeting PDCD4

Zhang, Yixi; Zhu, Zhi‐Jun; Huang, Shanzhou; Zhao, Qiang; Huang, Changjun; Tang, Yunhua; Sun, Chengjun; Zhang, Zhiheng; Wang, Linhe; Chen, Huadi; Chen, Maogen; Wang, Ju

doi:10.1186/s12935-019-0909-8

Cited by 44 publications

(36 citation statements)

References 32 publications

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“…25 Liu et al 26 have indicated that lncRNA MEG3 could inhibit cell proliferation and promote cell apoptosis in HCC. A study by Zhang et al 27 has confirmed that lncRNA XIST could promote cell proliferation and migration through targeting PDCD4 in HCC. In our present study, we investigated the effect of lncRNA RHPN1-AS1 on HCC cells and found that lncRNA RHPN1-AS1 could facilitate HCC cell proliferation, migration and invasion.…”

Section: Discussionmentioning

confidence: 94%

RETRACTED: LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

Song

Ren

et al. 2020

Technol Cancer Res Treat

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Hepatocellular carcinoma (HCC) is a severe disease with high mortality in the world. Emerging evidence has suggested that lncRNAs play an important role in cancer progression, including HCC. This study aimed to comprehensively investigate the effect of lncRNA RHPN1 antisense RNA 1 (RHPN1-AS1) on HCC and its underlying molecular mechanism. In this study, we evaluated the expressions of lncRNA RHPN1-AS1 and miR-7-5p by qRT-RCR in both HCC tissue and HCC cells. Our findings showed that lncRNA RHPN1-AS1 was upregulated in HCC tissue and HCC cells, while miR-7-5p was downregulated. LncRNA RHPN1-AS1 expression in HCC patients was closely related to vascular invasion, tumor-node-metastasis (TNM) stage and barcelona clinic liver cancer (BCLC) stage. Furthermore, we quantified cell clone-formation ability, proliferation, migration and invasion of HCCLM3 and MHCC97 H cells using several assays (colony formation assay, 5-Ethynyl-2′-deoxyuridine (EdU) assay and transwell assay, respectively). Functional experiments confirmed that silencing lncRNA RHPN1-AS1 inhibited cell proliferation, migration and invasion in HCCLM3 and MHCC97 H cells. After that, bioinformatics analysis, dual luciferase reporter gene assay, qRT-PCR and western blot were used to investigate the molecular mechanism of lncRNA RHPN1-AS1 on HCC. Mechanistically, the rescue experiments demonstrated that miR-7-5p inhibitor reversed the inhibition effect of silencing lncRNA RHPN1-AS1 on HCCLM3 cells proliferation, migration and invasion. Moreover, silencing lncRNA RHPN1-AS1 also inhibited the activation of PI3K/AKT/mTOR pathway. Taken together our findings demonstrated that lncRNA RHPN1-AS1 could facilitate cell proliferation, migration and invasion via targeting miR-7-5p and activating PI3K/AKT/mTOR pathway in HCC.

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Section: Discussionmentioning

confidence: 94%

RETRACTED: LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

Song

Ren

et al. 2020

Technol Cancer Res Treat

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“…In order to clarify the possible molecular mechanisms underlying the oncogenic effects of miR-183-5p in HCC, we carried out further mechanistic studies. Bioinformatics analysis and dual-luciferase reporter assays verified that PDCD4 was a downstream target of miR-183-5p, which was in consistence with previous reports regarding HCC [ 45 , 46 ]. Past researches have identified PDCD4 as a tumor suppressor in HCC [ 45 , 46 ].…”

Section: Discussionsupporting

confidence: 87%

“…Bioinformatics analysis and dual-luciferase reporter assays verified that PDCD4 was a downstream target of miR-183-5p, which was in consistence with previous reports regarding HCC [ 45 , 46 ]. Past researches have identified PDCD4 as a tumor suppressor in HCC [ 45 , 46 ]. Moreover, it was observed that PDCD4 expression was dramatically reduced in HCC tissues compared with paracancerous tissues and that an inverse correlation existed between miR-183-5p and PDCD4 expression.…”

Section: Discussionsupporting

confidence: 87%

MicroRNA-183-5p contributes to malignant progression through targeting PDCD4 in human hepatocellular carcinoma

Duan

et al. 2020

Bioscience Reports

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Hepatocellular carcinoma (HCC) remains one of the most common malignant tumors worldwide. This study aimed to investigate the biological role of microRNA-183-5p (miR-183-5p), a novel tumor-related miRNA, in HCC and illuminate the possible molecular mechanisms. The expression patterns of miR-183-5p in clinical samples were characterized using qPCR analysis. Kaplan-Meier survival curve was applied to evaluate the correlation between miR-183-5p expression and overall survival of HCC patients. Effects of miR-183-5p knockdown on HCC cell proliferation, apoptosis, migration and invasion capabilities were determined via CCK8 assays, flow cytometry, scratch wound healing assays and Transwell invasion assays, respectively. Mouse neoplasm transplantation models were established to assess the effects of miR-183-5p knockdown on tumor growth in vivo. Bioinformatics analysis, dual-luciferase reporter assays and rescue assays were performed for mechanistic researches. Results showed that miR-183-5p was highly expressed in tumorous tissues compared with adjacent normal tissues. Elevated miR-183-5p expression correlated with shorter overall survival of HCC patients. Moreover, miR-183-5p knockdown significantly suppressed proliferation, survival, migration and invasion of HCC cells compared with negative control treatment. Consistently, miR-183-5p knockdown restrained tumor growth in vivo. Furthermore, programmed cell death factor 4 (PDCD4) was identified as a direct target of miR-183-5p. Additionally, PDCD4 down-regulation was observed to abrogate the inhibitory effects of miR-183-5p knockdown on malignant phenotypes of HCC cells. Collectively, our data suggest that miR-183-5p may exert an oncogenic role in HCC through directly targeting PDCD4. The current study may offer some new insights for understanding the role of miR-183-5p in HCC.

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“…For example, in breast cancer, MIR210HG acts as ceRNA of miR-1226-3p to regulate the expression of mucin-1c, promoting the occurrence of metastasis; 21 in hepatocellular carcinoma, XIST regulates PDCD4 by targeting miR-497-5p to regulate the proliferation and migration of cancer cells. 22 In this study, we identified the interaction between miR-513b-5p with AZIN1-AS1. We observed that the expression level of miR-513b-5p increased significantly after AZIN1-AS1 knockdown, while the overexpression of AZIN1-AS1 increased the expression of miR-513b-5p.…”

Section: Discussionmentioning

confidence: 95%

<p>AZIN1-AS1, A Novel Oncogenic LncRNA, Promotes the Progression of Non-Small Cell Lung Cancer by Regulating MiR-513b-5p and DUSP11</p>

Cai

Liu

et al. 2020

OTT

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Background: Emerging researches have demonstrated that aberrantly expressed long noncoding RNAs (lncRNAs) have great significance in non-small cell lung cancer (NSCLC) progression. The aim of this study was to explore the role of lncRNA AZIN1 antisense RNA 1 (AZIN1-AS1) in NSCLC and the related mechanism. Methods: Expressions of AZIN1-AS1 and miR-513b-5p in NSCLC samples were detected by qRT-PCR. NSCLC cell lines (H1299 and HCC827) were used in vitro assays. CCK-8 assay, EdU assay, wound healing test and Transwell assay were carried out to test the biological influence of AZIN1-AS1 on NSCLC cells. Subcutaneous xenotransplanted tumor model and tail vein injection model were established to test the role of AZIN1-AS1 in vivo. Interactions between AZIN1-AS1 and miR-513b-5p, miR-513b-5p and dual-specificity phosphatase 11 (DUSP11) were determined by bioinformatic analysis, qRT-PCR, Western blot, and luciferase reporter assay. Results: AZIN1-AS1 was up-regulated in NSCLC cells and tissues, while miR-513b-5p was significantly down-regulated. Silencing of AZIN1-AS1 or overexpression of miR-513b-5p markedly inhibited proliferation, migration and invasion of NSCLC cells, while overexpression of AZIN1-AS1 or inhibition of miR-513b-5p functioned oppositely. Importantly, AZIN1-AS1 mediated the promotion of malignancy of NSCLC cells was reversed by miR-513b-5p mimics. What's more, AZIN1-AS1 could down-regulate miR-513b-5p via sponging it, and there existed a negative correlation between AZIN1-AS1 expression and miR-513b-5p expression in NSCLC samples. AZIN1-AS1 also enhanced the expression levels of DUSP11, which was proved as a target gene of miR-513b-5p. Further in vivo experiments showed that silencing of AZIN1-AS1 decreased tumor growth and metastasis, which was accompanied by overexpression of miR-513b-5p and inhibition of DUSP11 in tumor tissues. Conclusion: AZIN1-AS1 acts as a tumor promoter in NSCLC, which is ascribed to the regulation of miR-513b-5p and DUSP11.

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lncRNA XIST regulates proliferation and migration of hepatocellular carcinoma cells by acting as miR-497-5p molecular sponge and targeting PDCD4

Cited by 44 publications

References 32 publications

RETRACTED: LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

RETRACTED: LncRNA RHPN1-AS1 Promotes Cell Proliferation, Migration and Invasion Through Targeting miR-7-5p and Activating PI3K/AKT/mTOR Pathway in Hepatocellular Carcinoma

MicroRNA-183-5p contributes to malignant progression through targeting PDCD4 in human hepatocellular carcinoma

<p>AZIN1-AS1, A Novel Oncogenic LncRNA, Promotes the Progression of Non-Small Cell Lung Cancer by Regulating MiR-513b-5p and DUSP11</p>

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