The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1

Hou, Zhouhua; Xu, Xuwen; Zhou, Ledu; Fu, Xiaoyu; Tao, Shuhui; Zhou, Jiebin; Tan, Deming; Liu, Shuiping

doi:10.1177/1010428317718135

Cited by 61 publications

(73 citation statements)

References 50 publications

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“…Therefore, the identification of key lncRNAs associated with HCC is critical to clarify this disease and identify novel therapeutic targets. It is reported that lncRNA GAS5 is downregulated in HCC, and its overexpression can impede cell migration and invasion ; the expression of lncRNA HOTAIR in HCC is elevated, and patients with high expression of it have a poor prognosis ; moreover, the expression of lncRNA MALAT1 is also confirmed to be an independent prognostic factor for HCC . It is worth noting that the expression of DUXAP8 is closely related to the occurrence and progression of a variety of tumors.…”

Section: Discussionmentioning

confidence: 95%

“…The pathogenesis is a complex process with multiple factors and steps. Growing studies have shown that lncRNAs are abnormally expressed in human tumors, including HCC . Therefore, the identification of key lncRNAs associated with HCC is critical to clarify this disease and identify novel therapeutic targets.…”

Section: Discussionmentioning

confidence: 99%

“…Existing studies also report that lncRNA has important functions in HCC. For example, high expression of lncRNA MALAT1, promoting tumor proliferation and metastasis, is expected to be one of the potential HCC therapy targets . In recent years, the role of lncRNA double homeobox A pseudogene 8 (DUXAP8) has been gradually studied in cancers.…”

Section: Introductionmentioning

confidence: 99%

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Long noncoding RNA DUXAP8 contributes to the progression of hepatocellular carcinoma via regulating miR‐422a/PDK2 axis

et al. 2020

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Background Hepatocellular carcinoma (HCC) is one of the most deadly cancer worldwide. Multiple long noncoding RNAs (lncRNAs) are recently identified as crucial oncogenic factors or tumor suppressors. In this study, we explored the functon and mechanism of lncRNA double homeobox A pseudogene 8 (DUXAP8) in the progression of HCC. Methods Expression levels of DUXAP8 in HCC tissue samples were measured using qRT‐PCR. The association between pathological indexes and the expression of DUXAP8 was also analyzed. Human HCC cell lines SMMC‐7721 and QSG‐7701 were used in in vitro studies. CCK‐8 assay was used to assess the effect of DUXAP8 on HCC cell line proliferation. Scratch healing assay and Transwell assay were conducted to detect the effect of DUXAP8 on migration and invasion. Furthermore, dual‐luciferase reporter assay was used to confirm targeting relationship between miR‐422a and DUXAP8. Additionally, Western blot was used to detect the regulatory function of DUXAP8 on pyruvate dehydrogenase kinase 2 (PDK2). Results DUXAP8 expression HCC clinical samples was significantly increased and this was correlated with unfavorable pathological indexes. High expression of DUXAP8 was associated with shorter overall survival time of patients. Its overexpression remarkably facilitated the proliferation, metastasis, and epithelial‐mesenchymal transition of HCC cells. Accordingly, knockdown of it suppressed the malignant phenotypes of HCC cells. Overexpression of DUXAP8 significantly reduced the expression of miR‐422a by sponging it, but enhanced the expression of PDK2. Conclusions DUXAP8 was a sponge of tumor suppressor miR‐422a in HCC, enhanced the expression of PDK2 indirectly, and functioned as an oncogenic lncRNA.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

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Long noncoding RNA DUXAP8 contributes to the progression of hepatocellular carcinoma via regulating miR‐422a/PDK2 axis

et al. 2020

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“…Long noncoding RNAs (LncRNAs) are noncoding RNAs longer than 200 nucleotides . Accumulating evidence showed lncRNAs, such as MALAT1, HOTAIR, and H19, are associated with tumor proliferation, survival, and metastasis . lncRNA KCNQ1OT1, located on chromosome 11p15.5, which has been demonstrated that play a vital modulator in proliferation and metastasis of various tumors, such as cholangiocarcinoma, hepatocellular carcinoma, and breast cancer .…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA KCNQ1OT1 promotes proliferation, migration, and invasion in maxillary sinus squamous cell carcinoma by regulating miR‐204/EphA7 axis

Sun

et al. 2019

J of Cellular Biochemistry

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Long noncoding RNAs have been demonstrated to contribute to the development and progression of various cancers. However, the underlying regulatory mechanisms of KCNQ1OT1 in tumorigenesis of maxillary sinus squamous cell carcinoma (MSSCC) remain unknown. Herein, we found that KCNQ1OT1 expression was markedly upregulated in MSSCC tissues and MSSCC cell line (IMC‐3) by using quantitative reverse transcription‐polymerase chain reaction. Loss‐of‐function experiments revealed that the deletion of KCNQ1OT1 inhibited cell proliferation, migration, and invasion. Moreover, we confirmed KCNQ1OT1 could directly interact with miR‐204 by bioinformatic prediction and dual luciferase assay, and miR‐204 inhibitor markedly reversed MSSCC tumor phenotypes induced by shKCNQ1OT1. Finally, we demonstrated that KCNQ1OT1/miR‐204 facilitated MSSCC progression by regulating Eph receptor A7 (EphA7). Taken together, these results revealed a novel regulatory mechanism KCNQ1OT1/miR‐204/EphA7 axis, which could provide a new understanding of MSSCC tumorigenesis and develop potential targets for MSSCC therapy.

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“…6 MALAT1, H19, HULC, and HOTAIR have been found to act as oncogenes or tumor suppressors. [7][8][9] 2 | MATERIALS AND METHODS…”

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confidence: 99%

Long noncoding RNA NEAT1 promotes cell proliferation, migration, and invasion in hepatocellular carcinoma through interacting with miR‐384

Zhū

Yang

et al. 2018

J of Cellular Biochemistry

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It was reported that long non‐coding RNA nuclear‐enriched abundant transcript 1 (NEAT1) is involved in hepatocellular carcinoma (HCC). However, the underlying mechanism of tumorigenesis is still largely unclear. Here, we found that NEAT1 is remarkably upregulated in HCC tissues and cell lines. Overexpression of NEAT1 notably accelerated HCC cell proliferation, migration, and invasion. Knockdown of NEAT1 significantly inhibited HCC cell proliferation, migration and invasion. MiR‐384 expression was lower in HCC tissues and cell lines than adjacent nontumor tissues and L02 cell. MiR‐384 exhibited the functions of tumor‐suppressive. The expression of miR‐384 was negatively correlated with the expression of NEAT1. Overexpression of NEAT1 reduced miR‐384 expression, whereas inhibition of miR‐384 led to a distinct upregulation of NEAT1 expression. In addition, we provided evidence that miR‐384 was directly bound to the sequence of NEAT1 by luciferase reporter and RNA‐binding protein immunoprecipitation assays. Overexpression of miR‐384 inhibited NEAT1 function. Thus, we demonstrated that NEAT1 promotes the malignant biological properties of hepatocellular carcinoma by negatively regulating miR‐384.

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The long non-coding RNA MALAT1 promotes the migration and invasion of hepatocellular carcinoma by sponging miR-204 and releasing SIRT1

Cited by 61 publications

References 50 publications

Long noncoding RNA DUXAP8 contributes to the progression of hepatocellular carcinoma via regulating miR‐422a/PDK2 axis

Long noncoding RNA DUXAP8 contributes to the progression of hepatocellular carcinoma via regulating miR‐422a/PDK2 axis

Long noncoding RNA KCNQ1OT1 promotes proliferation, migration, and invasion in maxillary sinus squamous cell carcinoma by regulating miR‐204/EphA7 axis

Long noncoding RNA NEAT1 promotes cell proliferation, migration, and invasion in hepatocellular carcinoma through interacting with miR‐384

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