Long noncoding RNA UCA1 promotes tumour metastasis by inducing GRK2 degradation in gastric cancer

Wang, Zhenqiang; He, Changyu; Hu, Lei; Shi, Hui; Li, Jianfang; Gu, Qinxuan; Su, Liping; Liu, Bingya; Li, Chen; Zhu, Zhenggang

doi:10.1016/j.canlet.2017.08.013

Cited by 76 publications

(64 citation statements)

References 32 publications

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“…It was predicted that STAT3 can be provided as an miR-506 target. [23][24][25] LncRNA ILF3-AS1 can promote melanoma development through targeting miR-200b/a/429. LncRNAs are transcripts with more than 200 nucleotides and show no protein-coding capacity.…”

Section: Discussionmentioning

confidence: 99%

“…21 They are manifested to be involved in biological processes. [23][24][25] LncRNA MLLT4 antisense RNA 1 is decreased and can act as a potential indicator of poor prognosis in GC. [23][24][25] LncRNA ILF3-AS1 can promote melanoma development through targeting miR-200b/a/429.…”

Section: Discussionmentioning

confidence: 99%

“…26 LncRNA SNHG17 is able to promote cell proliferation by acting as an unfavorable prognostic indicator and epigenetically inhibiting P57 in colorectal cancer. [23][24][25] can play various roles in digestive system cancers and might be a possible prognostic biomarker in digestive system carcinoma patients. [23][24][25] LncRNA MLLT4 antisense RNA 1 is decreased and can act as a potential indicator of poor prognosis in GC.…”

Section: Discussionmentioning

confidence: 99%

“…22 For instance, lncRNA MALAT1 can promote osteosarcoma metastasis and proliferation by sponging miR-144-3p. [23][24][25] LncRNA ILF3-AS1 can promote melanoma development through targeting miR-200b/a/429. 26 LncRNA SNHG17 is able to promote cell proliferation by acting as an unfavorable prognostic indicator and epigenetically inhibiting P57 in colorectal cancer.…”

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confidence: 99%

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Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Tan

Wang

Liu

et al. 2019

J of Cellular Biochemistry

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Accumulating evidence has indicated that lncRNA NEAT1 exerts critical roles in cancers. So far, the detailed biological role and mechanisms of NEAT1 which are responsible for human gastric cancer (GC) is still largely unknown. Here, we observed that NEAT1 and STAT3 expression were significantly upregulated in human gastric cancer cells including BGC823, SGC-7901, AGS, MGC803 and MKN28 cells compared to normal gastric epithelial cells GES-1 while miR-506 was downregulated. We inhibited NEAT1 and observed that NEAT1 inhibition was able to repress the growth, migration and invasion of gastric cancer cells. Reversely, overexpression of NEAT1 exhibited an increase ability of gastric cancer progression in BGC823 and SGC-7901 cells. Bioinformatics analysis, dual luciferase reporter assays, RIP assays and RNA pull-down tests validated the negative binding correlation between NEAT1 and miR-506. In addition, it was found that miR-506 can modulate expression of NEAT1 in vitro. STAT3 was predicted as an mRNA target of miR-506 and miR-506 mimics can suppress STAT3 mRNA expression. Subsequently, it was observed that downregulation of NEAT1 can restrain gastric cancer development by decreasing STAT3 which can be reversed by miR-506 inhibitors. Therefore, it was hypothesized in our study that NEAT1 can be recognized as a ceRNA to modulate STAT3 by sponging miR-506 in gastric cancer. In conclusion, we implied that NEAT1 can serve as an important biomarker in gastric cancer diagnosis and treatment. This article is protected by copyright. All rights reserved.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Tan

Wang

Liu

et al. 2019

J of Cellular Biochemistry

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“…Alterations in certain oncogenes and tumor-suppressor genes finally lead to disordered cell proliferation, migration and invasion. 8,9 Long non-coding RNAs (lncRNAs), RNA molecules longer than 200 nucleotides, have an important role in gene regulation and cell function. 10 Major attention was attracted to long noncoding RNAs, thanks to its vital role involved in many molecular events, which usually contribute to the cancer progression.…”

Section: Introductionmentioning

confidence: 99%

<p>LncRNA MALAT1 Regulates the Cell Proliferation and Cisplatin Resistance in Gastric Cancer via PI3K/AKT Pathway</p>

Dai¹,

Zhang²,

Li³

2020

CMAR

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Background: Many studies showed that long non-coding RNA MALAT1 is served as an oncogene. However, the specific role of MALAT1 in gastric cancer is not fully elucidated. The aim of this study is to elucidate the regulatory effects of MALAT1 on tumor development and cisplatin resistance in gastric cancer. Methods: TCGA database was applied to investigate the expression levels of MALAT1 in GC tissues and normal gastric tissues and its correlation with GC patients' survival. Univariate and multivariate analysis were performed to investigate whether MALAT1 expression is an independent risk for overall survival of gastric cancer patients. The expression of MALAT1 was detected by Quantitative real-time PCR. After knockdown or overexpression of MALAT1, the cellular functions of GC cells were detected by cell-proliferation, flow cytometry, transwell assay and colony formation assays, respectively. Western blot analysis was performed to detect the protein levels of Bcl-2 and key genes in the PI3K/AKT pathway in GC cells. Finally, CCK-8 assay was performed to explore the effect of MALAT1 on cisplatin resistance of GC cells. Results: Higher expression of MALAT1 was detected in GC tissues than that of adjacent normal tissues, high MALAT1 expression is an independent risk for overall survival of gastric cancer patients. Knockdown of MALAT1 inhibited proliferation, migration and invasion of GC cells, while overexpression of MALAT1 Overexpression of MALAT1 yielded opposite results. Western blot results showed that protein expressions of p-PI3K, p-AKT and p-STAT3 were downregulated after MALAT1 knockdown in GC cells, while these proteins were upregulated after MALAT1 overexpression. Additionally, the IC 50 in MGC803/CDDP cells transfected with si-MALAT1 was lower than in those transfected with si-NC. The apoptotic rate in MGC803 cells transfected with pcDNA-MALAT1 was remarkably lower than those transfected with NC. Conclusion: We demonstrated that MALAT1 is highly expressed in GC, high MALAT1 expression is an independent risk factor for OS among GC patients. Moreover, MALAT1 promotes malignant progression of GC and contributes to cisplatin resistance of GC cells, indicating MALAT1 may serve as a biological hallmark for predicting the prognosis of GC.

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LncRNA UCA1/miR‐124 axis modulates TGFβ1‐induced epithelial‐mesenchymal transition and invasion of tongue cancer cells through JAG1/Notch signaling

Zhang

Liang

Liu

et al. 2019

J of Cellular Biochemistry

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Tongue cancer remains a massive threat to public health due to the high rate of metastasis. Tumor cell epithelial-mesenchymal transition (EMT), which can be induced by transforming growth factor β1 (TGFβ1), has been regarded as a significant contributor to cancer invasion and migration. In our previous study, long noncoding RNA (lncRNA) MALAT1/miR-124/JAG1 axis modulates the growth of tongue cancer. In addition to metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), another lncRNA, urothelial cancer associated 1 (UCA1), can promote EMT and cancer metastasis. In the present study, UCA1 was overexpressed in tongue cancer tissues and cell lines. UCA1 overexpression was correlated to the poorer prognosis of patients with tongue cancer. UCA1 knockdown significantly suppressed TGFβ1-induced tongue cancer cell invasion and EMT by decreasing vimentin and increasing E-cadherin.Regarding the molecular mechanism, UCA1 could directly bind to micro-RNA-124 (miR-124) and negatively regulate each other. UCA1 knockdown ameliorated, whereas miR-124 inhibition exacerbated TGFβ1-induced EMT and invasion in tongue cancer cells through miR-124 downstream jagged 1 (JAG1) and Notch signaling. Moreover, miR-124 inhibition partially impaired the effect of UCA1 knockdown. In tongue cancer tissues, miR-124 expression was remarkably decreased, whereas JAG1 mRNA expression was increased. miR-124 was negatively correlated with UCA1 and JAG1. UCA1 and JAG1 were positively correlated. In summary, we provided a novel mechanism by which the EMT process and cancer cell invasion in tongue cancer could be modulated from the perspective of lncRNA-miRNA-mRNA regulation. K E Y W O R D Sepithelial-mesenchymal transition, lncRNA urothelial cancer associated 1, miR-124, transforming growth factor β1, tongue cancer

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Long noncoding RNA UCA1 promotes tumour metastasis by inducing GRK2 degradation in gastric cancer

Cited by 76 publications

References 32 publications

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

Long noncoding RNA NEAT1‐modulated miR‐506 regulates gastric cancer development through targeting STAT3

<p>LncRNA MALAT1 Regulates the Cell Proliferation and Cisplatin Resistance in Gastric Cancer via PI3K/AKT Pathway</p>

LncRNA UCA1/miR‐124 axis modulates TGFβ1‐induced epithelial‐mesenchymal transition and invasion of tongue cancer cells through JAG1/Notch signaling

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