MicroRNA-137 Upregulation Increases Bladder Cancer Cell Proliferation and Invasion by Targeting PAQR3

Xiu, Youcheng; Liu, Zan; Xia, Shunyao; Jin, Chengjun; Yin, Huaifu; Zhao, Weiming; Wu, Qiong

doi:10.1371/journal.pone.0109734

Cited by 65 publications

(43 citation statements)

References 37 publications

(29 reference statements)

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“…recently also report that miR-137 suppresses tumor growth and metastasis in human hepatocellular carcinoma by targeting AKT2 (54). The studies from Shimuzu et al showed that ectopic expression of miR-137 suppresses bladder cancer cell proliferation (27), whereas another studies indicated that over-expression of miR-137 promotes cell proliferation, migration and invasion of bladder cancer cells (55). In our studies presented here, we found that miR-137 expression level in primary human bladder cancer tissues was dramatically down-regulated as compared with their paired adjacent non-tumorous tissues.…”

Section: Discussionmentioning

confidence: 99%

Induction of miR-137 by Isorhapontigenin (ISO) Directly Targets Sp1 Protein Translation and Mediates Its Anticancer Activity BothIn VitroandIn Vivo

Zeng

Zhou

et al. 2016

Molecular Cancer Therapeutics

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Our recent studies found that isorhapontigenin (ISO) showed a significant inhibitory effect on human bladder cancer cell growth, accompanied with cell cycle G0/G1 arrest as well as down-regulation of Cyclin D1 expression at transcriptional level via inhibition of Sp1 transactivation in bladder cancer cells. In current studies, the potential ISO inhibition of bladder tumor formation has been explored in xenograft nude mouse model, and the molecular mechanisms underlying ISO inhibition of Sp1 expression and anti-cancer activities has been elucidated both in vitro and in vivo. Moreover, the studies demonstrated that ISO treatment induced the expression of miR-137, which in turn suppressed Sp1 protein translation by direct targeting Sp1 mRNA 3′UTR. Similar to ISO treatment, ectopic expression of miR-137 alone led to G0/G1 cell growth arrest and inhibition of anchorage-independent growth in human bladder cancer cells, which could be completely reversed by over-expression of GFP-Sp1. The inhibition of miR-137 expression attenuated ISO-induced the inhibition of Sp1/Cyclin D1 expression, and induction of G0/G1 cell growth arrest and suppression of cell anchorage-independent growth. Taken together, our studies have demonstrated that miR-137 induction by ISO targets Sp1 mRNA 3′UTR and inhibits Sp1 protein translation, which consequently results in reduction of Cyclin D1 expression, induction of G0/G1 growth arrest and inhibition of anchorage-independent growth in vitro and in vivo. Our results have provided novel insights into understanding the anti-cancer activity of ISO in the therapy of human bladder cancer.

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Section: Discussionmentioning

confidence: 99%

Induction of miR-137 by Isorhapontigenin (ISO) Directly Targets Sp1 Protein Translation and Mediates Its Anticancer Activity BothIn VitroandIn Vivo

Zeng

Zhou

et al. 2016

Molecular Cancer Therapeutics

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“…miRNAs can regulate cell proliferation, cell differentiation, apoptosis by interfering (mainly inhibiting) gene expression at the posttranscriptional level and thus indicate an important role in cancer development and progression Hu et al, 2014;Kavitha et al, 2014;Orang and Barzegari, 2014). Many studies have investigated that miRNAs were deregulated in various types of human cancer (Guo et al, 2013;Xiu et al, 2014). DICER is a member of RNase enzymes and an important nuclease responsible for the cleavage of miRNA precursors (Liu et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Association between the DICER rs1057035 Polymorphism and Cancer Risk: Evidence from a Meta-analysis of 1,2675 Individuals

Yu¹,

Kuang²,

Yin³

2015

Asian Pacific Journal of Cancer Prevention

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Background: DICER, one of the microRNA (miRNA) biogenesis proteins, is involved in the maturation of miRNAs and is implicated in cancer development and progression. The results from previous epidemiological studies on associations between DICER rs1057035 polymorphism and cancer risk were inconsistent. Thereforewe performed this meta-analysis to summarize possible associations. Materials and Methods: We searched all relevant articles on associations between DICER rs1057035 polymorphism and cancer risk from PubMed, EMBASE, Chinese Biomedical Literature and Chinese National Knowledge Infrastructure until August 2014. Odds ratios (ORs) with 95% confidence intervals (CIs) were calculated to assess any associations. Heterogeneity tests, sensitivity analyses and publication bias assessments were also performed in this meta-analysis. All analyses were conducted using STATA software. Results: Seven case-control studies, including 4,875 cancer cases and 7,800 controls were included in the meta-analysis. Overall, the results indicated that the C allele of DICER rs1057035 polymorphism was significantly associated with decreased cancer risk in allelic comparison, heterozygote and dominant genetic models (C vs T: OR=0.88, 95%CI 0.81-0.95, p=0.002; TC vs TT: OR=0.85, 95%CI 0.77-0.93, p=0.001; CC/TC vs TT: OR=0.86, 95%CI 0.78-0.94, p=0.001). In the subgroup analysis by ethnicity, a significantly decreased cancer risk was found in Asian but not Caucasian populations. Conclusions: The present meta-analysis suggests that the C allele of the DICER rs1057035 polymorphism probably decreases cancer risk. However, this association may be Asian-specific and the results should be treated with caution. Further well-designed studies based on larger sample sizes and group of populations are needed to validate these findings.

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“…Moreover, PAQR3 repressed cell proliferation, migration, sprouting, and angiogenesis of endothelial cells [13]. Furthermore, PAQR3 played a tumor suppressive role in the tumorigenesis of colorectal cancers, bladder cancer, and hepatocellular carcinoma [10,[16][17][18]. However, the role of PAQR3 in the LSCC remains unknown.…”

Section: Introductionmentioning

confidence: 99%

PAQR3 plays a suppressive role in laryngeal squamous cell carcinoma

Zhuang

2015

Tumor Biol.

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Laryngeal squamous cell carcinoma (LSCC) is a common type of head and neck malignancy worldwide. The molecular mechanism of LSCC remains not well understood. PAQR3 (progestin and AdipoQ receptors) is a member of the progestin and adipoQ receptor (PAQR) family. Many studies have showed that PAQR3 acts as a new tumor suppressor. However, its expression and functions in LSCC are still unknown. In our study, the expression of PAQR3 was downregulated in human LSCC tissues compared to that in adjacent tissues. Moreover, overexpression of PAQR3 suppressed LSCC cell proliferation and invasion. In addition, PAQR3 inhibited cell proliferation and invasion by regulating ERK phosphorylation. In conclusion, our data demonstrated that PAQR3 acted a tumor suppressive role in LSCC, providing a novel diagnostic and therapeutic option for LSCC in the future.

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MicroRNA-137 Upregulation Increases Bladder Cancer Cell Proliferation and Invasion by Targeting PAQR3

Cited by 65 publications

References 37 publications

Induction of miR-137 by Isorhapontigenin (ISO) Directly Targets Sp1 Protein Translation and Mediates Its Anticancer Activity BothIn VitroandIn Vivo

Induction of miR-137 by Isorhapontigenin (ISO) Directly Targets Sp1 Protein Translation and Mediates Its Anticancer Activity BothIn VitroandIn Vivo

Association between the DICER rs1057035 Polymorphism and Cancer Risk: Evidence from a Meta-analysis of 1,2675 Individuals

PAQR3 plays a suppressive role in laryngeal squamous cell carcinoma

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