LincRNA-p21 activates endoplasmic reticulum stress and inhibits hepatocellular carcinoma

Yang, Ning; Fu, Yong; Zhang, Haibin; Sima, Hui; Zhu, Nan; Yang, Guang-Shun

doi:10.18632/oncotarget.4661

Cited by 65 publications

(42 citation statements)

References 32 publications

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“…Besides, ADAM10 is the target gene of miR‐122‐5p and the higher expression of ADAM10 is revealed in breast cancer tissue than that of normal tissue . A previous study demonstrated that lincRNA is closely linked with the development and progression of HCC . However, LINC01551 expression in HCC and its significance remain largely unknown.…”

Section: Introductionmentioning

confidence: 99%

Retracted: Long noncoding LINC01551 promotes hepatocellular carcinoma cell proliferation, migration, and invasion by acting as a competing endogenous RNA of microRNA‐122‐5p to regulate ADAM10 expression

Gao

Yin

et al. 2019

J of Cellular Biochemistry

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Hepatocellular carcinoma (HCC) is a severe disease with high mortality in the world. It has been shown that long noncoding RNA (lncRNA) might play a role in HCC. The aim of the present study was to identify the role of long intergenic noncoding RNA 01551 (LINC01551) in the HCC development and explore the underlying mechanism of LINC01551/miR‐122‐5p/ADAM10 axis. The differentially expressed lncRNAs associated with HCC were screened out by a microarray analysis. The expression of LINC01551, miR‐122‐5p, and ADAM10 was determined in HCC tissues and cells. The potential miRNA (miR‐122‐5p) regulated by LINC01551 was explored, and the target relationship between miR‐122‐5p and ADAM10 was confirmed. To evaluate the effect of LINC01551 and miR‐122‐5p on proliferation, migration, invasion, and apoptosis of HCC, different plasmids were delivered into MHCC97‐H cells. High expression of LINC01551 and ADAM10 yet low‐expression of miR‐122‐5p were revealed in HCC tissues and cells. Overexpression of miR‐122‐5p could downregulate ADAM10. Biological prediction websites and fluorescence in situ hybridization assay verified that LINC01551 was mainly expressed in the cytoplasm. Silencing LINC01551 reduced HCC cell viability, proliferation, migration, invasion, and cell cycle entry yet induce cell apoptosis. Upregulation of LINC01551 increased its ability of competitively binding to miR‐122‐5p, thus reducing miR‐122‐5p and upregulating ADAM10 expression, as well as promoting the proliferative, migrative, and invasive ability. Taken together the results, it is highly possible that LINC01551 functions as an competing endogenous RNA (ceRNA) to regulate the miRNA target ADAM10 by sponging miR‐122‐5p and therefore promotes the development of HCC, highlighting a promising competitive new target for the HCC treatment.

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Section: Introductionmentioning

confidence: 99%

Retracted: Long noncoding LINC01551 promotes hepatocellular carcinoma cell proliferation, migration, and invasion by acting as a competing endogenous RNA of microRNA‐122‐5p to regulate ADAM10 expression

Gao

Yin

et al. 2019

J of Cellular Biochemistry

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“…For example, lnc-EGFR accelerates T-regulatory cell differentiation leading to immune evasion of HCC [6], and a variety of lncRNAs, such as MALT1 [7], TP73-AS1 [8], HULC [9], XIST [10], and HOTAIR [11], function as oncogenes, promoting HCC growth and metastasis by regulating miRNA or proteins. However, lncRNA uc.134 and lincRNA-p21 inhibit HCC progression by repressing CUL4A-mediated ubiquitination of LATS1 [12] or activating endoplasmic reticulum stress [13]. These findings indicate lncRNAs are potential prognostic factors for HCC.…”

Section: Introductionmentioning

confidence: 92%

lncRNA SNHG8 Promotes the Tumorigenesis and Metastasis by Sponging miR-149-5p and Predicts Tumor Recurrence in Hepatocellular Carcinoma

Dong

Teng

Guo

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long noncoding RNAs (lncRNAs) are aberrantly expressed in multiple malignant tumors involved in tumor growth and metastasis. Accumulating data show that small nucleolar RNA host gene (SNHG) 1/12/20 plays a key role in the progression of hepatocellular carcinoma (HCC). However, the molecular mechanisms by which SNHG8 contributes to HCC remain elusive and merit exploration. Methods: The association between SNHG8 expression and the clinicopathological characteristics and prognoses in HCC patients was analysed by using qRT-PCR analysis and the data from The Cancer Genome Atlas. Cell growth and metastatic potential were determined by MTT, colony formation, Transwell assays, and the mouse xenograft tumor model and lung metastasis model. Epithelial–mesenchymal transition markers were detected by western blot analysis. The binding capacity of SNHG8 with miRNAs was evidenced by bioinformatic analysis and a luciferase reporter assay. In addition, the rescue experiments were performed based on co-transfection with sh-SNHG8 and a miR-149 inhibitor in HCC cells. Results: The expression levels of lncRNA SNHG8 were dramatically increased in HCC tissues and cell lines as compared with the adjacent normal tissues, and SNHG8 expression was an independent prognostic factor of tumor recurrence in HCC patients. Furthermore, knockdown of SNHG8 inhibited cell proliferation, invasion, and lung metastasis in vitro and in vivo, whereas overexpression of SNHG8 reversed these effects. SNHG8 acted as a sponge of miR-149 and counteracted the tumor suppressive effects of mi R-149 in HCC cells. Expression of phosphatase, Mg2+/Mn2+ dependent 1F, a target of R-149, displayed a negative correlation with miR-149 expression but a positive correlation with SNHG8 expression in HCC specimens. Conclusion: As lncRNA SNHG8 may promote HCC tumorigenesis and metastasis by sponging miR-149, it is a potential candidate marker and therapeutic target for HCC.

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“…LncRNA-p21 acts as a transcriptional suppressor in the p53 pathway by activating p53 to promote apoptosis [113]. It has been investigated that lncRNAp21 is deregulated in various human diseases, such as skin tumors, prostatic cancers, and HCCs [114][115][116]. It also functions as a tumor suppressor in malignancies, but the mechanism of the process remains elusive [115].…”

Section: Lncrnap21mentioning

confidence: 99%

LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma

Kim

Park

Lee

2020

IJMS

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Long non-coding RNAs (lncRNAs) are emerging as important contributors to the biological processes underlying the pathophysiology of various human diseases, including hepatocellular carcinoma (HCC). However, the involvement of these molecules in chronic liver diseases, such as nonalcoholic fatty liver disease (NAFLD) and viral hepatitis, has only recently been considered in scientific research. While extensive studies on the pathogenesis of the development of HCC from hepatic fibrosis have been conducted, their regulatory molecular mechanisms are still only partially understood. The underlying mechanisms related to lncRNAs leading to HCC from chronic liver diseases and cirrhosis have not yet been entirely elucidated. Therefore, elucidating the functional roles of lncRNAs in chronic liver disease and HCC can contribute to a better understanding of the molecular mechanisms, and may help in developing novel diagnostic biomarkers and therapeutic targets for HCC, as well as in preventing the progression of chronic liver disease to HCC. Here, we comprehensively review and briefly summarize some lncRNAs that participate in both hepatic fibrosis and HCC.

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LincRNA-p21 activates endoplasmic reticulum stress and inhibits hepatocellular carcinoma

Cited by 65 publications

References 32 publications

Retracted: Long noncoding LINC01551 promotes hepatocellular carcinoma cell proliferation, migration, and invasion by acting as a competing endogenous RNA of microRNA‐122‐5p to regulate ADAM10 expression

Retracted: Long noncoding LINC01551 promotes hepatocellular carcinoma cell proliferation, migration, and invasion by acting as a competing endogenous RNA of microRNA‐122‐5p to regulate ADAM10 expression

lncRNA SNHG8 Promotes the Tumorigenesis and Metastasis by Sponging miR-149-5p and Predicts Tumor Recurrence in Hepatocellular Carcinoma

LncRNAs Act as a Link between Chronic Liver Disease and Hepatocellular Carcinoma

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