Re-expression of miR-199a suppresses renal cancer cell proliferation and survival by targeting GSK-3β

Tsukigi, Masaaki; Bilim, Vladimir; Yuuki, Kaori; Ugolkov, Andrey; Naito, Sei; Nagaoka, Akira; Kato, Tomoyuki; Motoyama, Teiichi; Tomita, Yoshihiko

doi:10.1016/j.canlet.2011.10.008

Cited by 83 publications

(76 citation statements)

References 30 publications

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“…It is well documented that inducible miR-199a-5p arrests cell proliferation and contributes to cell death (7,8,26,27). Our group and others have previously reported that miR-199a-5p regulates cellular detoxifying systems by targeting multidrug resistance-associated protein 1 (6) and CD44 (12).…”

Section: Discussionmentioning

confidence: 96%

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

Chan

Roy

Huang

et al. 2012

Journal of Biological Chemistry

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Background:The role of miR-199a-5p in angiogenesis remains unclear. Results: miR-199a-5p exerts angiostatic effects by targeting Ets-1-MMP1 pathway and is down-regulated in skin wound healing. Conclusion: Down-regulation of miR-199a-5p switches on wound angiogenesis through derepressing of Ets-1-MMP1 pathway. Significance: This investigation provides novel mechanistic insight explaining miR-dependent regulation of wound angiogenesis and the foundation of developing therapeutic intervention in treating chronic nonhealing wounds.

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Section: Discussionmentioning

confidence: 96%

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

Chan

Roy

Huang

et al. 2012

Journal of Biological Chemistry

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“…Recent research also found that miR-199a-5p can promote gastric cancer by inhibition of Klotho protein expression (He et al, 2014). Besides, can modulate the process of renal fibrosis (Christian et al, 2013) and the growth of kidney cancer cells (Tsukigi et al, 2012). Additionally, miR-199a-5p plays a regulatory role in the TLR4/NF-kB inflammation signaling pathways induced by lipopolysaccharides (Liu et al, 2013).…”

Section: Introductionmentioning

confidence: 95%

The function of miR-199a-5p/Klotho regulating TLR4/NF-κB p65/NGAL pathways in rat mesangial cells cultured with high glucose and the mechanism

Chen

et al. 2015

Molecular and Cellular Endocrinology

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“…One was chromosome 19 for miR-199a-1 and the other one was chromosome 1 for miR-199a-2. It is reported that miR-199a-5p inhibited cell proliferation and induced cell death [20, 21]. Based on these findings, we sought to investigate the functional implications of miR-199a-5p in breast cancer both in vivo and in vitro.…”

Section: Introductionmentioning

confidence: 99%

miR-199a-5p confers tumor-suppressive role in triple-negative breast cancer

et al. 2016

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BackgroundTriple-negative breast cancer (TNBC) remains a poor prognostic factor for breast cancer since no effective targeted therapy is readily available. Our previous studies confirmed miR-199a-5p is a TNBC-specific circulating biomarker, however, its functional roles in breast cancer is largely unknown. Thus, we investigated the functional implication of miR-199a-5p in TNBC and its potential underlying mechanisms.MethodsMTT assay was performed to investigate the cell proliferation after transient transfection of miR-199a-5p in MDA-MB-231 cell line, followed by cell cycle analysis. Transwell invasion assay and wound healing assay were used to study the invasion and migration ability respectively. To further investigate the stemness-related characteristics of miR-199a-5p in breast cancer cells, single-cell clonogenic assay and aldehyde dehydrogenase (ALDH) assay were performed. 32 normal and 100 breast cancer patients’ plasma were recruited to identify the potential circulating markers by qPCR.ResultsCell proliferation assay revealed significant inhibition after miR-199a-5p ectopic expression (p < 0.0001), as a result of decreased S phase (p = 0.0284), increased G0/G1 phase (p = 0.0260) and apoptosis (p = 0.0374). Invasiveness (p = 0.0005) and wound healing ability were also decreased upon miR-199a-5p overexpression. It significantly altered EMT-related genes expression, namely CDH1, ZEB1 and TWIST. Single-cell clonogenic assay showed decreased colonies in miR-199a-5p (p = 0.0182). Significant downregulation (p = 0.0088) and inhibited activity (p = 0.0390) of ALDH was observed in miR-199a-5p. ALDH1A3, which is the dominant isoform of ALDH, is significantly upregulated in breast cancer plasma especially in TNBC (p = 0.0248). PIK3CD was identified as a potential downstream target of miR-199a-5p.ConclusionsTaken together, we unraveled, for the first time, the tumor-suppressive role of miR-199a-5p in TNBC, which attributed to EMT and cancer stemness properties, providing a novel therapeutic options towards this aggressive disease.

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Re-expression of miR-199a suppresses renal cancer cell proliferation and survival by targeting GSK-3β

Cited by 83 publications

References 30 publications

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

The MicroRNA miR-199a-5p Down-regulation Switches on Wound Angiogenesis by Derepressing the v-ets Erythroblastosis Virus E26 Oncogene Homolog 1-Matrix Metalloproteinase-1 Pathway

The function of miR-199a-5p/Klotho regulating TLR4/NF-κB p65/NGAL pathways in rat mesangial cells cultured with high glucose and the mechanism

miR-199a-5p confers tumor-suppressive role in triple-negative breast cancer

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