Long non-coding RNAs in hepatocellular carcinoma: Potential roles and clinical implications

Niu, Zhaojian; Niu, Xiao-Jun; Wang, Wenhong

doi:10.3748/wjg.v23.i32.5860

Cited by 55 publications

(68 citation statements)

References 176 publications

(180 reference statements)

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“…Furthermore, MALAT1 was been shown to affects cell viability, proliferation and migration, colony formation, cell cycle distribution, and tumor growth in CaSki cervical cancer cells [23]. MALAT1 has also been reported to be an oncogene in HCC, in addition, MALAT1 was been found play a marker with high sensitivity for HCC at both early and late stages [24], suggesting that it can be used as a potential diagnostic tool for HCC [25]. Moreover, a study reported that inhibition of MALAT1 in HepG2 cells could effectively reduce cell viability, motility, invasiveness, and increase the sensitivity to apoptosis [26].…”

Section: Discussionmentioning

confidence: 99%

Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma

Pan

Tong

Cui

et al. 2018

Cell Physiol Biochem

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Background/Aims: Hepatocellular carcinoma (HCC) has a high morbidity as well as mortality and is believed to be one of the most prevalent cancers worldwide. The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in numerous cancers, including HCC. This study aimed to explore the role of MALAT1 in HCC progression. Methods: The expression levels of MALAT1 and Vimentin in HCC tissues and relative pair-matched adjacent normal liver tissues were analyzed by RT-PCR, and immunohistochemistry. Using bioinformatics analysis and dual-luciferase assay, we examined the correlation between MALAT1 and miR-30a-5p. Dual-luciferase assay and western blotting suggested that Vimentin was a target of miR-30a-5p. A wound healing assay and transwell assays were employed to determine the effect of MALAT1 and miR-30a-5p on cell migration and invasion in HCC. Results: Our data demonstrated that the levels of MALAT1 and Vimentin were upregulated in HCC tissues and that miR-30a-5p was a direct target of MALAT1. Silenced MALAT1 and overexpressed miR-30a-5p each inhibited cell migration and invasion. Additionally, dual-luciferase assay and western blotting demonstrated that MALAT1 could competitively sponge miR-30a-5p and thereby regulate Vimentin. Conclusion: Our data suggest that MALAT1 acts as an oncogenic lncRNA that promotes HCC migration and invasion. Therefore, the MALAT1-miR-30a-5p-Vimentin axis is a potential therapeutic target and molecular biomarker in HCC.

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Section: Discussionmentioning

confidence: 99%

Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma

Pan

Tong

Cui

et al. 2018

Cell Physiol Biochem

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“…Long non-coding RNAs (lncRNAs) are a subgroup of non-coding RNA (ncRNAs) transcripts, which are greater than 200 nucleotides in length, with little or no protein-coding potential [1,2]. While lncRNAs are emerging as important contributors to the biological processes underlying the pathophysiology of various human diseases, including inflammation and neoplasia [3], the involvement of these molecules in chronic liver diseases, such as viral hepatitis and nonalcoholic fatty liver disease (NAFLD), has only been considered in scientific research [3].…”

Section: Introductionmentioning

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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“…Long non‐coding RNAs (lncRNAs) have been demonstrated to matter much in the aetiology of glioma, breast cancer, hepatocellular carcinoma, prostate cancer and retinoblastoma 7, 8, 9, 10. Mounting evidences also indicated that lncRNAs could serve as proto‐oncogenes or anti‐oncogenes by regulating tumour‐related genes or pathways 11, 12.…”

Section: Introductionmentioning

confidence: 99%

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

Yang

et al. 2018

J Cellular Molecular Medi

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Since lncRNAs could modulate neoplastic development by modulating downstream miRNAs and genes, this study was carried out to figure out the synthetic contribution of HOTAIR, miR‐613 and c‐met to viability, apoptosis and proliferation of retinoblastoma cells. Totally 276 retinoblastoma tissues and tumour‐adjacent tissues were collected, and human retinoblastoma cell lines (ie, Y79, HXO‐Rb44, SO‐Rb50 and WERI‐RB1) were also gathered. Moreover, transfections of pcDNA3.1‐HOTAIR, si‐HOTAIR, miR‐613 mimic, miR‐613 inhibitor, pcDNA3.1/c‐met were performed to evaluate the influence of HOTAIR, miR‐613 and c‐met on viability, apoptosis and epithelial‐mesenchymal transition (EMT) of retinoblastoma cells. Dual‐luciferase reporter gene assay was also arranged to confirm the targeted relationship between HOTAIR and miR‐613, as well as between miR‐613 and c‐met. Consequently, up‐regulated HOTAIR and down‐regulated miR‐613 expressions displayed associations with poor survival status of retinoblastoma patients (P < 0.05). Besides, inhibited HOTAIR and promoted miR‐613 elevated E‐cadherin expression, yet decreased Snail and Vimentin expressions (P < 0.05). Simultaneously, cell proliferation and cell viability were also less‐motivated (P < 0.05). Nonetheless, c‐met prohibited the functioning of miR‐613, resulting in promoted cell proliferation and viability, along with inhibited cell apoptosis (P < 0.05). Finally, HOTAIR was verified to directly target miR‐613, and c‐met was the direct target gene of miR‐613 (P < 0.05). In conclusion, the role of lncRNA HOTAIR/miR‐613/c‐met signalling axis in modulating retinoblastoma cells’ viability, apoptosis and expressions of EMT‐specific proteins might provide evidences for developing appropriate diagnostic and treatment strategies for retinoblastoma.

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Long non-coding RNAs in hepatocellular carcinoma: Potential roles and clinical implications

Cited by 55 publications

References 176 publications

Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma

Long Non-Coding MALAT1 Functions as a Competing Endogenous RNA to Regulate Vimentin Expression by Sponging miR-30a-5p in Hepatocellular Carcinoma

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

LncRNA HOTAIR/miR‐613/c‐met axis modulated epithelial‐mesenchymal transition of retinoblastoma cells

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