LncRNA MALAT1 induces colon cancer development by regulating miR‐129‐5p/HMGB1 axis

Wu, Qiong; Wu, Meng; Jin, Ying; Zhao, Haijian

doi:10.1002/jcp.26383

Cited by 146 publications

(110 citation statements)

References 41 publications

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“…The diminished expression of miR‐129 in MM cell lines was further explored. MiR‐129 was reported previously to be regulated by lncRNAs . In this study, we for the first time demonstrated a direct link between PCAT‐1 and miR‐129 in MM and that the PCAT‐1 level in MM‐derived PCs was significantly higher than that in the control and negatively associated with the level of serum miR‐129.…”

Section: Discussionsupporting

confidence: 62%

PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma

Shen

Kong

Yang

et al. 2020

J Cellular Molecular Medi

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Loss of one or some specific miRNA‐mediated regulation is closely associated with malignant progression of multiple myeloma (MM). But how these miRNAs work and what role the specific miRNA plays in this process of malignant progression remain unclear. It was found in this study that the expression of miR‐129 was decreased in both MM cell lines and newly diagnosed MM patients. Further clinicopathological statistics showed that miR‐129 was correlated with the isotype of MM patients. MiR‐129 overexpression disturbed cell proliferation, cell cycle evolution and spurred apoptosis both in vitro and in vivo. MAP3K7, a kinase able to activate NF‐κB circuit, was found to be up‐regulated in MM and contain a binding target of miR‐129. In addition, lncRNA PCAT‐1 functioned to sponge miR‐129 and thereby lowered its expression. PCAT‐1 knockdown eliminated the tumour‐promoting effect caused by miR‐129 inhibition, probably through repressing MAP3K7 and subsequent NF‐κB activation. To the best of our knowledge, this is the first study to have discovered that increased expression of PCAT‐1 could augment cell proliferation and cycle procession and inhibit apoptosis by down‐regulating miR‐129 via the MAP3K7/NF‐κB pathway in MM.

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Section: Discussionsupporting

confidence: 62%

PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma

Shen

Kong

Yang

et al. 2020

J Cellular Molecular Medi

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“…[3][4][5][6][7][8][9] LncRNAs are noncoding RNAs with a length of more than 200 nt, as ceRNAs, which further regulated the production of downstream proteins by regulating the miRNA/mRNA axis. [10][11][12][13] Some lncRNAs have been reported to be differentially expressed in colorectal cancer tissues and cells, but their functions have been verified. 14 For example, lncRNA DLEU1 promoted CRC cell progression through regulating KPNA3.…”

Section: Introductionmentioning

confidence: 99%

<p>HNF1A-AS1 Regulates Cell Migration, Invasion and Glycolysis via Modulating miR-124/MYO6 in Colorectal Cancer Cells</p>

Guo¹,

Zhang²,

Liu³

et al. 2020

OTT

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Background: Accumulating evidence determined that lncRNAs play multiple roles in cell progression in colorectal cancer (CRC). Long noncoding RNA (lncRNA) hepatocyte nuclear factor 1 homeobox A (HNF1A)-antisense RNA 1 (AS1) has been identified to affect cell growth and disease diagnosis in various cancers, including CRC. However, the underlying regulatory mechanism of HNF1A-AS1 in cell progression and glycolysis has not been fully explored in CRC. Materials and Methods: The expression of HNF1A-AS1, microRNA-124 (miR-124) and Myosins of class VI (MYO6) was detected using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The analysis of glucose consumption, lactate production and hexokinase 2 (HK2) protein level was used to assess glycolysis in cells. The protein level of HK2 and MYO6 was measured with Western blot. Cell migration and invasion were evaluated using the transwell assay. The relationship among HNF1A-AS1, miR-124 and MYO6 was determined via luciferase reporter and RNA immunoprecipitation (RIP) assay. Results: In this study, we found that HNF1A-AS1 was upregulated in CRC tissues and cell lines. Functional experiments determined that reduction of HNF1A-AS1 or promotion of miR-124 inhibited cell migration and invasion as well as glycolysis in CRC cells. What' more, luciferase reporter assay manifested that miR-124 was a target of HNF1A-AS1 and MYO6 was a target mRNA of miR-124 in CRC cells. Additionally, reverse experiments showed that the effects of si-HNF1A-AS1 on colorectal cancer cells were impaired by anti-miR-124 and the effects of high miR-124 expression on CRC cells were rescued by upregulating MYO6. HNF1A-AS1 regulated MYO6 expression via targeting miR-124 in CRC cells. Conclusion: In this study, we first found that HNF1A-AS1 regulated cell migration, invasion and glycolysis via modulating miR-124/MYO6 in CRC cells.

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“…miR-129-5p participated in a ceRNA pathway in colon cancer. 35 miR-181a-5p and multiple myeloma progression. 36 All above examples showed the interaction between miRNAs and mRNA in cancers.…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG16 drives proliferation, migration, and invasion of hemangioma endothelial cell through modulation of miR‐520d‐3p/STAT3 axis

Zhao

Fu²,

Zhang

et al. 2018

Cancer Medicine

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It has been verified that long noncoding RNAs (lncRNAs) have great effects on various biological behaviors of human diseases. Although more and more lncRNAs have been studied in human cancers, countless lncRNAs still need to be excavated. This study aims to investigate the impacts of lncRNA SNHG16 on proliferation and metastasis of human hemangioma endothelial cell (HemECs). qRT‐PCR analysis was carried out to explore the expression pattern of SNHG16, miR‐520d‐3p, and STAT3. The effect of SNHG16 on cell proliferation was detected by MTT and colony formation assay. Flow cytometry analysis was performed to test the apoptosis of HemECs cells. Migration and invasion of HemECs cells were determined and examined by transwell assays. Tube formation assay helped to observe the influence of SNHG16 expression on the vasoformation of HemECs cells. The correlations among SNHG16, miR‐520d‐3p, and STAT3 were certified by bioinformatics analysis, pull‐down assay, and dual‐luciferase reporter assay. Finally, rescue assays were conducted to demonstrate the effects of SNHG16‐miR‐520d‐3p‐STAT3 axis on biological behaviors of HemECs cell. SNHG16 was strongly expressed in proliferating phase hemangioma tissues and HemECs cells. Silenced SNHG16 negatively affected proliferation, migration, and invasion of HemECs cell. LncRNA SNHG16 acted as a ceRNA to upregulate STAT3 through binding with miR‐520d‐3p in HemECs cell. LncRNA SNHG16 acted as a ceRNA to drive proliferation, vasoformation, migration, and invasion of HemECs cells through modulating miR‐520d‐3p/STAT3 axis.

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LncRNA MALAT1 induces colon cancer development by regulating miR‐129‐5p/HMGB1 axis

Cited by 146 publications

References 41 publications

PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma

PCAT‐1 promotes cell growth by sponging miR‐129 via MAP3K7/NF‐κB pathway in multiple myeloma

<p>HNF1A-AS1 Regulates Cell Migration, Invasion and Glycolysis via Modulating miR-124/MYO6 in Colorectal Cancer Cells</p>

LncRNA SNHG16 drives proliferation, migration, and invasion of hemangioma endothelial cell through modulation of miR‐520d‐3p/STAT3 axis

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