LncRNA-SVUGP2 suppresses progression of hepatocellular carcinoma

Hu, Jiangfeng; Song, Chenlin; Duan, Bensong; Zhang, Xiaoyan; Li, Dongliang; Zhu, Liang; Gao, Hengjun

doi:10.18632/oncotarget.18279

Cited by 21 publications

(20 citation statements)

References 51 publications

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“…Given the crucial role of lncRNAs in biology and etiology, further identification of novel lncRNAs underlying NSCLC development is imperative. LncRNA-SVUGP2 is recently found to have a decreased expression in hepatocellular carcinoma samples and can exhibit tumour-suppressive effects in this malignancy [27]. However, the possible impact of lncRNA-SVUGP2 in other cancers including NSCLC is largely unknown.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Repression of lncRNA-SVUGP2 mediated by EZH2 contributes to the development of non-small cell lung cancer via brisking Wnt/β-catenin signal

Wei

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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To grab the possible impact of lncRNA-SVUGP2 in the biology and process of non-small cell lung cancer (NSCLC). Sixty paired NSCLC tumour and the adjacent non-tumour lung tissues were collected for detection of lncRNA-SVUGP2. lncRNA-SVUGP2 expression in NSCLC cells (SK-MES-1, A549, SPC-A1, and NCI-H1975) was also detected. lncRNA-SVUGP2 was overexpressed and depressed in A549 and H1975 cells, and the effects of lncRNA-SVUGP2 dysregulation on cell biological performances including viability, colony formation, apoptosis, migration and invasion were grabbed. Furthermore, the regulatory association of lncRNA-SVUGP2 vs. EZH2 in H1975 cells, as well as the association between lncRNA-SVUGP2 and Wnt/b-catenin pathway, was explored. lncRNA-SVUGP2 was depressed in NSCLC tissues and cells. Overexpression of lncRNA-SVUGP2 depressed proliferation, induced apoptosis, and suppressed migration and invasion of A549 and H1975 cells. In addition, lncRNA-SVUGP2 was repressed by EZH2 and was inversely correlated with EZH2 levels in H1975 cells. Repression of lncRNA-SVUGP2 potentially participated in the oncogenic function of EZH2. Besides, overexpression of lncRNA-SVUGP2 depressed the briskness of Wnt/b-catenin signal in H1975 cells. Our data reveal that lncRNA-SVUGP2 is under-expressed in NSCLC cells and the reduced expression of lncRNA-SVUGP2 may enhance the development and process of NSCLC by interacting with EZH2 and activating Wnt/b-catenin pathway. ARTICLE HISTORY KEYWORDSNon-small cell lung cancer; lncRNA-SVUGP2; EZH2; Wnt/b-catenin signal CONTACT Sen Wei

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Repression of lncRNA-SVUGP2 mediated by EZH2 contributes to the development of non-small cell lung cancer via brisking Wnt/β-catenin signal

Wei

Liu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…For example, overexpression of lncRNA-SVUGP2 inhibits the proliferation, migration and invasion of HepG2 and Hep3B HCC cells. 33 It is reported that EGOT plays an oncogenic role in gastric cancer and could be used as a diagnostic and prognostic biomarker. 14 In the present study, we observed that EGOT was significantly highly expressed in HCC cells than that in adjacent normal tissues, which may be associated with elevated markers of advanced malignancies.…”

Section: Discussionmentioning

confidence: 99%

<p>Long Non-Coding RNA EGOT Promotes the Malignant Phenotypes of Hepatocellular Carcinoma Cells and Increases the Expression of HMGA2 via Down-Regulating miR-33a-5p</p>

Wu¹,

Ai²,

Zhang³

et al. 2019

OTT

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Background: Chronic hepatitis C virus (HCV) infection is an important risk factor for hepatocellular carcinoma (HCC). EGOT is a long non-coding RNA (lncRNA) induced after HCV infection that increases viral replication by antagonizing the antiviral response. Interestingly, EGOTalso acts as a crucial regulator in multiple cancers. However, its role in HCC remains unclear. Methods: Real-time PCR (RT-PCR) was used to detect the expression of EGOT in HCC samples and cell lines. CCK-8 assay and colony formation assay were performed to evaluate the effect of EGOT on proliferation. Scratch healing assay and transwell assay were used to detect the changes of migration and invasion. Flow cytometry was used to detect the effect of EGOT on apoptosis. Interaction between EGOT and miR-33a-5p was determined by bioinformatics analysis, RT-PCR, and dual-luciferase reporter assay. Western blot was used to confirm that high mobility group protein A2 (HMGA2) could be modulated by EGOT. Results: Compared with normal liver tissues, the expression level of EGOT in HCC tissues was significantly up-regulated. EGOT markedly regulated viability, migration and invasion of HCC cells. The expression level of EGOT was negatively correlated the expression level of miR-33a-5p. It is also confirmed that EGOT could specifically bind to miR-33a-5p and could reduce its expression, in turn, up-regulate the expression of HMGA2. Conclusion: Our data imply that EGOT may be a novel therapeutic target for HCC, and highlights the key role of EGOT/miR-33a-5p/HMGA2 in the progression of this deadly disease.

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“…The method of colony formation experiment referred to the previous research . Cells were seeded into a 3.5 cm dishes at a density of 2000 per dish and cultured in an incubator.…”

Section: Methodsmentioning

confidence: 99%

Epidermal growth factor‐containing fibulin‐like extracellular matrix protein 1 (EFEMP1) suppressed the growth of hepatocellular carcinoma cells by promoting Semaphorin 3B(SEMA3B)

Duan

Jiang

et al. 2019

Cancer Medicine

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Aim Epidermal growth factor‐containing fibulin‐like extracellular matrix protein 1(EFEMP1) has been found to be involved in the occurrence and development of many cancers. The relationship between EFEMP1 and the development of hepatocellular carcinoma (HCC) and the molecular mechanism are not fully understood. Methods Real‐time polymerase chain reaction (PCR) and tissue microarray were used to detect the expression of EFEMP1 in HCC cell lines and tissue. Methylation‐specific PCR assay was used to measure the methylation level of EFEMP1 in HCC cell lines and tissue. To study the function of EFEMP1 on cell function, Huh7 and HepG2 were infected with lentiviral particles expressing EFEMP1. MTT assay and colony formation assay were used to examine the effect of EFEMP1 on cell proliferation. Annexin‐VAPC/7‐AAD double were used to detect the effect of EFEMP1 on cell apoptosis. To further detect the effect of EFEMP1 on the development of HCC in vivo, we performed the tumor formation experiment in nude mice. Gene chip was used to detect the expression profile of Huh7 and HepG2 overexpressing EFEMP1. To further screen out the differences, GO analysis and pathway analysis were performed. To study the effects of SEMA3B, specific siRNA was used to inhibit the expression of SEMA3B. Chi‐squared test and rank sum test were used to analyze the relationship between EFEMP1 expression and HCC clinical characteristic. Results The study found that the expression of EFEMP1 was significantly decreased in HCC cell lines and HCC tissues. The expression level of EFEMP1 was related to the TNM (the extent of the tumor, the extent of spread to the lymph nodes, the presence of metastasis) stage and the prognosis of patients with HCC. The decrease of protein expression suggested that the patient prognosis was worse, and the protein level of EFEMP1 may be an independent factor in the prognosis of HCC patients. Promoter methylation may be one of the reasons for EFEMP1 inhibition. EFEMP1 could inhibit the proliferation of HCC cells and promoted the apoptosis of HCC cells to regulate the development of HCC. And EFEMP1 promoted the apoptosis of HCC cells mainly through the mitochondrial apoptosis pathway. EFEMP1 may inhibit the proliferation of HCC cells through the SEMA3B gene in the Axon guidance pathway. Conclusion In summary, our research revealed the regulation of EFEMP1 on cell proliferation and apoptosis in HCC. EFEMP1 may suppress the growth of HCC cells by promoting SEMA3B.

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LncRNA-SVUGP2 suppresses progression of hepatocellular carcinoma

Cited by 21 publications

References 51 publications

RETRACTED ARTICLE: Repression of lncRNA-SVUGP2 mediated by EZH2 contributes to the development of non-small cell lung cancer via brisking Wnt/β-catenin signal

RETRACTED ARTICLE: Repression of lncRNA-SVUGP2 mediated by EZH2 contributes to the development of non-small cell lung cancer via brisking Wnt/β-catenin signal

<p>Long Non-Coding RNA EGOT Promotes the Malignant Phenotypes of Hepatocellular Carcinoma Cells and Increases the Expression of HMGA2 via Down-Regulating miR-33a-5p</p>

Epidermal growth factor‐containing fibulin‐like extracellular matrix protein 1 (EFEMP1) suppressed the growth of hepatocellular carcinoma cells by promoting Semaphorin 3B(SEMA3B)

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