The UCA1/miR-204/Sirt1 axis modulates docetaxel sensitivity of prostate cancer cells

Wang, Xu; Yang, Bo; Ma, Baojing

doi:10.1007/s00280-016-3158-8

Cited by 60 publications

(45 citation statements)

References 24 publications

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“…47,48 Recent studies showed that SIRT1 is a target for miR-204 and is functionally critical for multiple cancer phenotypes such as migration/invasion, EMT, and resistance to anoikis. 17,49,50 Consistent with these studies, we showed that both MALAT1 and SIRT1 bound to the same site on miR-204, and therefore, in addition to targeting miR-204 to Ago2-mediated silencing, MALAT1 may also compete with SIRT1 for binding to miR-204, both mechanisms releasing SIRT1 from the negative control by miR-204. In addition, SIRT1 is functionally critical for HCC migration/ invasion, supporting that miR-204-SIRT1 axis mediates the activity of MALAT1 on HCC migration/invasion.…”

Section: Discussionsupporting

confidence: 87%

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

Hou

Zhou

et al. 2017

Tumour Biol.

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Increasing evidence supports the significance of long non-coding RNA in cancer development. Several recent studies suggest the oncogenic activity of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in hepatocellular carcinoma. In this study, we explored the molecular mechanisms by which MALAT1 modulates hepatocellular carcinoma biological behaviors. We found that microRNA-204 was significantly downregulated in sh-MALAT1 HepG2 cell and 15 hepatocellular carcinoma tissues by quantitative real-time polymerase chain reaction analysis. Through bioinformatic screening, luciferase reporter assay, RNA-binding protein immunoprecipitation, and RNA pull-down assay, we identified microRNA-204 as a potential interacting partner for MALAT1. Functionally, wound-healing and transwell assays revealed that microRNA-204 significantly inhibited the migration and invasion of hepatocellular carcinoma cells. Notably, sirtuin 1 was recognized as a direct downstream target of microRNA-204 in HepG2 cells. Moreover, si-SIRT1 significantly inhibited cell invasion and migration process. These data elucidated, by sponging and competitive binding to microRNA-204, MALAT1 releases the suppression on sirtuin 1, which in turn promotes hepatocellular carcinoma migration and invasion. This study reveals a novel mechanism by which MALAT1 stimulates hepatocellular carcinoma progression and justifies targeting metastasis-associated lung adenocarcinoma transcript 1 as a potential therapy for hepatocellular carcinoma.

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Section: Discussionsupporting

confidence: 87%

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

Hou

Zhou

et al. 2017

Tumour Biol.

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“…UCA1 protected prostate cancer against apoptosis by sponging miR-184, leading to up-regulation of B-cell lymphoma/ leukemia 2 [127]. Silent mating type information regulation 2 homologue 1 (Sirt1) and activating transcription factor-2 (ATF2) are the downstream targets of miR-204 [128][129][130]. Silent mating type information regulation 2 homologue 1 (Sirt1) and activating transcription factor-2 (ATF2) are the downstream targets of miR-204 [128][129][130].…”

Section: Prostate Cancermentioning

confidence: 99%

“…Silent mating type information regulation 2 homologue 1 (Sirt1) and activating transcription factor-2 (ATF2) are the downstream targets of miR-204 [128][129][130]. In addition, the UCA1-miR-204-Sirt1 axis also contributed to resistance to docetaxel, which is a standard chemotherapy for patients with metastatic prostate cancer [128,131]. In addition, the UCA1-miR-204-Sirt1 axis also contributed to resistance to docetaxel, which is a standard chemotherapy for patients with metastatic prostate cancer [128,131].…”

Section: Prostate Cancermentioning

confidence: 99%

“…It was also found that UCA1 promoted prostate cancer cell proliferation and invasion via inhibition of miR-204. Silent mating type information regulation 2 homologue 1 (Sirt1) and activating transcription factor-2 (ATF2) are the downstream targets of miR-204 [128][129][130]. Sirt1 and ATF2 when up-regulated by UCA1 facilitate metastasis and proliferation of prostate cancer, respectively [128][129][130].…”

Section: Prostate Cancermentioning

confidence: 99%

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Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Xuan

Zhang

et al. 2019

FEBS Letters

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Long non-coding RNAs (lncRNAs) are a major subset of highly conserved non-coding RNAs (ncRNAs) that consist of at least 200 nucleotides and have limited protein-coding potential. Cumulative data have shown that lncRNAs are deregulated in many types of cancer and may control pathophysiological processes of cancer at various levels, including transcription, post-transcription and translation. Recently, lncRNAs have been demonstrated to interact with microRNAs (miRNAs), another major subset of ncRNAs, which regulate physiological and pathological processes by inhibiting target mRNA translation or promoting mRNA degradation. The lncRNA urothelial carcinomaassociated 1 (UCA1) has recently gained much attention as it is overexpressed in many types of cancer and is involved in carcinogenesis. Here, we review the crosstalk between UCA1 and miRNAs during the pathogenesis of cancer, with a focus on cancer-cell proliferation, invasion, drug resistance, and metabolism.

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“…Thus, our results suggested that the UCA1/miR‐204/SIRT1 axis can regulate cell proliferation and apoptosis in AML cells, which may be involved in AML malignant progression. A recent study has shown that inhibition of the UCA1/miR‐204/Sirt1 axis enhances the docetaxel sensitivity of prostate cancer cells by inducing apoptosis . Despite these promising results, a question about whether the UCA1/miR‐204/Sirt1 axis is involved in the chemosensitivity of AML cells remains unknown.…”

Section: Discussionmentioning

confidence: 99%

Silencing of lncRNA UCA1 curbs proliferation and accelerates apoptosis by repressing SIRT1 signals by targeting miR‐204 in pediatric AML

Zhang

et al. 2020

J Biochem & Molecular Tox

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The long noncoding RNA urothelial carcinoma‐associated 1 (UCA1) has been reported to sustain the proliferation of acute myeloid leukemia (AML) cells through downregulating cell cycle regulators p27kip1. Yet, the foundational mechanism of UCA1 in AML pathologies remains unclear. Herein, we found an escalation of UCA1 expression and suppression of miR‐204 expression in pediatric AML patients and cells. UCA1 silencing suppressed cell proliferative abilities, promoted apoptotic rates, decreased Ki67, and increased cleaved caspase‐3 in AML cells. Moreover, UCA1 sponged miR‐204 and suppressed its expression. UCA1 overexpression inversed the miR‐204 suppressed proliferation and promoted apoptosis. UCA1 also boosted the expression of SIRT1, a miR‐204 target, via the sponging interaction. Furthermore, miR‐204 inhibited inducible nitric oxide synthase and cyclooxygenase‐2 expression, while UCA1 overexpression inversed the inhibitory effects in AML cells. Our findings concluded that UCA1 downregulation repressed cell proliferation and promoted apoptosis through inactivating SIRT1 signals by upregulating miR‐204 in pediatric AML.

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The UCA1/miR-204/Sirt1 axis modulates docetaxel sensitivity of prostate cancer cells

Abstract: There is a UCA1/miR-204/Sirt1 axis in LNCaP and 22RV1 cells. The UCA1/miR-204/Sirt1 axis plays an important role in modulating in vitro docetaxel sensitivity of the prostate cancer cells.

Cited by 60 publications

References 24 publications

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

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

Crosstalk between the lncRNA UCA1 and microRNAs in cancer

Silencing of lncRNA UCA1 curbs proliferation and accelerates apoptosis by repressing SIRT1 signals by targeting miR‐204 in pediatric AML

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