lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR‐181b

Cui, Bingzhou; Li, Baoshan; Liu, Qi; You-qiang, Cui

doi:10.1002/jcb.26116

Cited by 89 publications

(65 citation statements)

References 41 publications

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“…Emerging evidence has indicated that lncRNA could sponge miRNA and regulate the functions of miRNAs . Previous studies also indicated that MALAT1 presented various functions as miRNA sponges in different cancers.…”

Section: Discussionmentioning

confidence: 99%

LncRNA MALAT1/miR‐129 axis promotes glioma tumorigenesis by targeting SOX2

Zhang

Wang

et al. 2018

J Cellular Molecular Medi

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We aimed to explore the interaction among lncRNA MALAT1, miR‐129 and SOX2. Besides, we would investigate the effect of MALAT1 on the proliferation of glioma stem cells and glioma tumorigenesis. Differentially expressed lncRNAs in glioma cells and glioma stem cells were screened out with microarray analysis. The targeting relationship between miR‐129 and MALAT1 or SOX2 was validated by dual‐luciferase reporter assay. The expressions of MALAT1, miR‐129 and SOX2 mRNA in both glioma non‐stem cells and glioma stem cells were examined by qRT‐PCR assay. The impact of MALAT1 and miR‐129 on glioma stem cell proliferation was observed by CCK‐8 assay, EdU assay and sphere formation assay. The protein expression of SOX2 was determined by western blot. The effects of MALAT1 and miR‐129 on glioma tumour growth were further confirmed using xenograft mouse model. The mRNA expression of MALAT1 was significantly up‐regulated in glioma stem cells compared with non‐stem cells, while miR‐129 was significantly down‐regulated in glioma stem cells. MALAT1 knockdown inhibited glioma stem cell proliferation via miR‐129 enhancement. Meanwhile, miR‐129 directly targeted at SOX2 and suppressed cell viability and proliferation of glioma stem cells by suppressing SOX2 expression. The down‐regulation of MALAT1 and miR‐129 overexpression both suppressed glioma tumour growth via SOX2 expression promotion in vivo. MALAT1 enhanced glioma stem cell viability and proliferation abilities and promoted glioma tumorigenesis through suppressing miR‐129 and facilitating SOX2 expressions.

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Section: Discussionmentioning

confidence: 99%

LncRNA MALAT1/miR‐129 axis promotes glioma tumorigenesis by targeting SOX2

Zhang

Wang

et al. 2018

J Cellular Molecular Medi

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“…For instance, Wang et al have found that DLEU1 contributes to ovarian carcinoma tumourigenesis and progression by interacting with miR‐490‐3p and altering CDK1 expression. Cui et al have reported that lncRNA CCAT1 promotes glioma tumourigenesis by sponging miR‐181b, thereby leading to derepression of its endogenous targets FGFR3 and PDGFRα; these findings point to a potential therapeutic target in glioma . A recent study verified that LINC00312 is associated with miR‐197‐3p and modulates the expression of a miR‐197‐3p target, p120, thereby providing powerful evidence that LINC00312 enhances gene expression at the post‐transcriptional level .…”

Section: Discussionmentioning

confidence: 94%

“…22 promotes glioma tumourigenesis by sponging miR-181b, thereby leading to derepression of its endogenous targets FGFR3 and PDGFRα; these findings point to a potential therapeutic target in glioma. 23,24 A recent study verified that LINC00312 is associated with miR-197-3p and modulates the expression of a miR-197-3p target, p120, thereby providing powerful evidence that LINC00312 enhances gene expression at the post-transcriptional level. 20 Here, we revealed a potential binding site within LINC00312 and miR-21 by bioinformatic prediction.…”

Section: Discussionmentioning

confidence: 97%

LINC00312 represses proliferation and metastasis of colorectal cancer cells by regulation of miR‐21

Wang

et al. 2018

J Cellular Molecular Medi

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Long non‐coding RNAs (lncRNAs) have emerged as important regulators of cancer, including colorectal cancer (CRC). The exact expression pattern of long intergenic noncoding RNA 00312 (LINC00312) in CRC and its mechanisms of action have not been reported. Here, we found that LINC00312 is underexpressed in CRC tissues and cell lines. Functional experiments suggested that LINC00312 suppresses growth, migration and invasion of CRC cells in vitro and attenuates tumour proliferation and metastasis in vivo. Mechanistically, LINC00312 was found to regulate the malignancy of CRC cells by binding to miR‐21 and by functioning as a tumour suppressor targeting PTEN. Overexpression of miR‐21 or knockdown of PTEN attenuated the LINC00312‐mediated inhibition of CRC cell proliferation and invasion. Taken together, our results elucidate the role of the LINC00312–miR‐21–PTEN axis in CRC cell proliferation and tumour progression and may lead to new lncRNA‐based diagnostics or therapeutics for CRC.

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“…[25][26][27][28] To reveal possible binding miRNA on CCAT1, we analysed the CCAT1 sequence using miRbase (http:// www.mirbase.org/search.shtml) and identified that miR-30c-2-3p could be sponged by CCAT1 ( Figure 3A). [25][26][27][28] To reveal possible binding miRNA on CCAT1, we analysed the CCAT1 sequence using miRbase (http:// www.mirbase.org/search.shtml) and identified that miR-30c-2-3p could be sponged by CCAT1 ( Figure 3A).…”

Section: Ccat1 Acts As a Sponge Of Mir-30c-2-3p In Hcc Cellsmentioning

confidence: 99%

“…Many studies have shown that CCAT1 could function as miRNA sponge in different cancers. [25][26][27][28] To reveal possible binding miRNA on CCAT1, we analysed the CCAT1 sequence using miRbase (http:// www.mirbase.org/search.shtml) and identified that miR-30c-2-3p could be sponged by CCAT1 ( Figure 3A). Next, we could like to address whether miR-30c-2-3p could bind CCAT1 in HCC.…”

Section: Ccat1 Acts As a Sponge Of Mir-30c-2-3p In Hcc Cellsmentioning

confidence: 99%

Upregulated LncRNA‐CCAT1 promotes hepatocellular carcinoma progression by functioning as miR‐30c‐2‐3p sponge

Zhang

Cai

Jiang

et al. 2019

Cell Biochemistry & Function

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Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related death over the world. It is well studied that long noncoding RNA colon cancer-associated transcript-1 (CCAT1) played important roles in variety of cancers promoting cell proliferation and metastasis by acting as a competing endogenous RNA (ceRNA) of microRNAs. However, whether CCAT1 could regulate HCC by serving as a ceRNA of microRNA remains to be revealed. In this study, we demonstrated that CCAT1 was highly expressed in HCC tissues and remarkably associated with metastasis. With a bioinformatics prediction and functional assay validation, we found a binding site of miR-30c-2-3p on CCAT1, which was important for CCAT1 to promote cell proliferation. Interestingly, we further revealed a novel recognition site for miR-30c-2-3p on the 3′UTR of CCNE1 by mutative method, luciferase assay, and cell viability confirmation. In general, CCAT1 regulate the expression of CCNE1 by acting as a ceRNA to sponge miR-30c-2-3p in regulating the cell proliferation of HCC. These results suggest that CCAT1 may be a new therapy target for HCC in the future.Significance of the study: Our findings may broaden the understanding of the role of CCAT1 in tumorigenesis and may provide a new therapy target for HCC.

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lncRNA CCAT1 Promotes Glioma Tumorigenesis by Sponging miR‐181b

Cited by 89 publications

References 41 publications

LncRNA MALAT1/miR‐129 axis promotes glioma tumorigenesis by targeting SOX2

LncRNA MALAT1/miR‐129 axis promotes glioma tumorigenesis by targeting SOX2

LINC00312 represses proliferation and metastasis of colorectal cancer cells by regulation of miR‐21

Upregulated LncRNA‐CCAT1 promotes hepatocellular carcinoma progression by functioning as miR‐30c‐2‐3p sponge

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