MicroRNA-16 suppresses epithelial-mesenchymal transition-related gene expression in human glioma

Wang, Qin; Xu, Li; Zhu, Yu; Yang, Ping

doi:10.3892/mmr.2014.2583

Cited by 40 publications

(46 citation statements)

References 8 publications

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“…Glioblastoma is characterized as extensive brain invasion [4,5], whose underlying molecular mechanisms were not elucidated in detail. To our interest, it is reported that the epithelial-mesenchymal transition (EMT) is implicated in the development and metastasis of glioblastoma [6], resulting in the migration and invasion of cancer cells from the primary focus. Till now, the detailed mechanisms have not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

Yao

Song

et al. 2015

Mol Neurobiol

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In recent decades, the chemokine receptor CXCR4 and its ligand CXCL12 have been extensively reported to be associated with tumorigenesis. In addition, Twist signaling induces the epithelial-mesenchymal transition (EMT) process in glioblastoma development. In the present study, in vitro assays were used to investigate the role of CXCR4 and Twist in human glioblastoma. We explored the impact of CXCR4 and Twist on human glioblastoma using in vitro protein and gene assays. We found the administration of CXCL12 upregulated the expression of p-ERK, p-AKT, Twist, N-cadherin, and MMP9 in U87 cells, whereas the increase of E-cadherin protein was affected. Subsequently, Twist activity and EMT signaling were directly influenced by PD98059 and LY294002. Most importantly, the genetic silencing of Twist inhibited CXCL12-induced EMT occurrence, including proliferation, migration, and tumor formation of U87 cells. In conclusion, CXCL12/CXCR4 pathway activates ERK and PI3K/AKT signaling to upregulate Twist pathway, leading to the progression of EMT in human glioblastoma. Our study creates a new stage for molecule-targeted therapy of human glioblastoma.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

Yao

Song

et al. 2015

Mol Neurobiol

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“…Several studies have shown the inhibitory effect of miR‐16 on tumorigenicity of different cancer cells through suppression of proliferation, invasion, migration, angiogenesis, and induction of apoptosis . Also, miR‐16 suppresses the expression of TGF‐β and some epithelial–mesenchymal transition (EMT)‐related genes . The aim of this study was to assess the impact of exogenous mature miR‐16 on both reprogramming and tumorigenicity of human breast cancer cells, which are under the influence of miR‐302/367 overexpression, and whether miR‐16 can serve as an effective adjuvant for tumor‐suppressive function of miR‐302/367.…”

Section: Introductionmentioning

confidence: 99%

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

2020

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Overexpression of either miR‐302 or miR‐302/367 cluster induces reprogramming of cancer cells and exerts tumor‐suppressive effects by induction of mesenchymal‐to‐epithelial transition, apoptosis and a less proliferative capacity. Several reports have described miR‐16 as a tumor suppressor microRNA (miRNA). Here, we studied the impact of exogenous induction of miR‐16 in MDA‐MB‐231 and SK‐BR‐3 breast cancer cells following overexpression of miR‐302/367 cluster and investigated whether transfection of these cells by a mature miR‐16 mimic could affect the reprogramming state of the cells and their tumorigenicity. miR‐16 enhanced the expression levels of OCT4A, SOX2, and NANOG, generally known as transcription or pluripotency factors, and suppressed proliferation and invasiveness of these cells. Meanwhile, inhibition of miR‐16 counteracted both the reprogramming effect and the antitumor function of miR‐302/367 in the breast cancer cells. Current results indicate that miR‐16 can work as an adjuvant to improve both cancer cell reprogramming and tumor‐suppressive function of miR‐302/367 cluster in MDA‐MB‐231 and SK‐BR‐3 cells, while its inhibition counteracts all of these effects. Combined application of miRNAs that share some common targets in cancer cell signaling pathways may provide new approaches for repression of multiple hallmarks of cancer.

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“…Some of the roles of miR-34 have already been discussed, as one of its targets is Smad4. As previously described, miR-16 inhibits TGF-β-induced EMT by silencing p-FAK and p-Akt expression, disrupting NF-κB and Slug transcriptional activity (Wang et al 2014 b ). Although it is not possible to assess the clinical efficacy of the miR-based therapeutics at this stage, these two drugs were well tolerated with minimal inflammatory side effects.…”

Section: Clinical Applications Of Mirs In Ovarian Prostate and Breasmentioning

confidence: 80%

“…In further cross-talk within the EMT regulators, Snail1 assists in the transcriptional repression of miR-200f, to enhance EMT (Diaz-Lopez et al 2015). Importantly, miR-16 and miR-200 family members silences TGF-β signaling and blocks EMT (Brabletz & Brabletz 2010, Wang et al 2014 b , Tang et al 2016). Individuals have the potential to influence several mRNA targets to regulate cancer progression (Davis-Dusenbery and Hata 2010).…”

Section: Mirs Impact Epithelial–mesenchymal Transdifferentiationmentioning

confidence: 99%

MicroRNA applications for prostate, ovarian and breast cancer in the era of precision medicine

Smith

Agarwal

Bhowmick

2017

Endocrine-Related Cancer

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The high degree of conservation in microRNA from Caenorhabditis elegans to humans has enabled relatively rapid implementation of findings in model systems to the clinic. The convergence of the capacity for genomic screening being implemented in the prevailing precision medicine initiative and the capabilities of microRNA to address these changes holds significant promise. However, prostate, ovarian and breast cancers are heterogeneous and face issues of evolving therapeutic resistance. The transforming growth factor-beta (TGFβ) signaling axis plays an important role in the progression of these cancers by regulating microRNAs. Reciprocally, microRNAs regulate TGFβ actions during cancer progression. One must consider the expression of miRNA in the tumor microenvironment a source of biomarkers of disease progression and a viable target for therapeutic targeting. The differential expression pattern of microRNAs in health and disease, therapeutic response and resistance has resulted in its application as robust biomarkers. With two microRNA mimetics in ongoing restorative clinical trials, the paradigm for future clinical studies rests on the current observational trials to validate microRNA markers of disease progression. Some of today’s biomarkers can be translated to the next generation of microRNA-based therapies.

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MicroRNA-16 suppresses epithelial-mesenchymal transition-related gene expression in human glioma

Cited by 40 publications

References 8 publications

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

RETRACTED ARTICLE: CXCL12/CXCR4 Axis Upregulates Twist to Induce EMT in Human Glioblastoma

miR‐16 enhances miR‐302/367‐induced reprogramming and tumor suppression in breast cancer cells

MicroRNA applications for prostate, ovarian and breast cancer in the era of precision medicine

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