RETRACTED: MicroRNA-1246 inhibits cell invasion and epithelial mesenchymal transition process by targeting CXCR4 in lung cancer cells

Xu, Xiaohui; Cao, Lei; Zhang, Ye; Lian, Hongjian; Sun, Zhiwei; Cui, Yuming

doi:10.3233/cbm-170317

Cited by 39 publications

(30 citation statements)

References 31 publications

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“…14 In contrast, miR-1246 inhibited cell invasion and epithelial mesenchymal transition (EMT) in lung cancer by targeting CXCR4. 15 These findings indicate that the role of miR-1246 depends on the type of human cancers. In this study, we mainly investigated the role of miR-1246 in melanoma.…”

Section: Introductionmentioning

confidence: 91%

<p>MicroRNA-1246 Promotes Melanoma Progression Through Targeting FOXA2</p>

Yu¹,

Yu²,

Sun³

2020

OTT

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Section: Introductionmentioning

confidence: 91%

<p>MicroRNA-1246 Promotes Melanoma Progression Through Targeting FOXA2</p>

Yu¹,

Yu²,

Sun³

2020

OTT

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“…MiRNA regulates the gene expression at the post-transcriptional level by binding at the 3ʹUTR of mRNA and thus inhibits the protein expression. MiR-1246 plays an important role in breast cancer [12], and inhibits cell invasion and epithelial-mesenchymal transition in lung cancer [13]. The previous study revealed that miR-1246 was down-regulated in CRNV, and overexpressed miR-1246 could significantly inhibit the proliferation of HUVEC [14].…”

Section: Introductionmentioning

confidence: 99%

lncRNA MIAT suppression alleviates corneal angiogenesis through regulating miR-1246/ACE

et al. 2019

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Corneal neovascularization (CRNV) is a prevalence eye disorder that affects the transparency and refraction properties of eyes. To explore the correlation between the level of Angiotensin II (Ang II) and corneal angiogenesis, the rat model of CRNV was established using alkali-burn, while the human umbilical vein endothelial cells (HUVECs) were stimulated using VEGF to induce the CRNV cells in vitro. RNA immunoprecipitation (RIP) and RNA pull-down were performed to validate the relationship between MIAT and miR-1246. The expression of MIAT and Ang II was increased, while miR-1246 was decreased in CRNV rat model. VEGF stimulation significantly promoted cell proliferation and migration of HUVECs, knockdown of MIAT dramatically reversed the effects of VEGF, while cells co-transfected with miR-1246 inhibitor obviously abolished the effect of VEGF+si-MIAT, however, enalaprilat abolished the effects of VEGF+si-MIAT+miR-1246 inhibitor. MIAT directly regulated the expression of miR-1246. In conclusion, VEGF stimulation promoted cell proliferation and migration of HUVECs mainly through regulating MIAT/miR-1246/ACE. ARTICLE HISTORY

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“…However, there exists a wide range of different opinions on whether miR‐1246 promotes or blunts the tumorigenesis. Xu et al documented that miR‐1246 prevents cell penetration as well as epithelial mesenchymal transition procedure by pursuing CXCR4 in lung cancer cells . Bhagirath et al established that miR‐1246 may be a tumor repressor in aggressive prostate cancer that is released via sEV from tumor cells, causing its upregulated expression in body fluids .…”

Section: Introductionmentioning

confidence: 99%

Lack of miR‐1246 in small extracellular vesicle blunts tumorigenesis of laryngeal carcinoma cells by regulating Cyclin G2

et al. 2020

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Small extracellular vesicle (sEV) has precise impacts on tumor microenvironment and play vital functions in intercellular interaction. However, the functional role of sEV miRNA on laryngeal squamous cell carcinoma (LSCC) is largely unresolved. Here, the expression of miR‐1246 in LSCC tissues and plasma sEV was examined. The internalization ability of sEV was determined by uptake assay. Then, the source and purity of sEV were checked through RNase and/or pharmacological inhibitors application. The invasion, migration, proliferation, and cell cycle assays were used to determine the altered abilities of miR‐1246 in sEV in LSCC. Finally, target gene of miR‐1246, Cyclin G2 (CCNG2), was stained immunohistochemically. In addition, the relationship between CCNG2 and clinicopathological features of patients was analyzed. We found that miR‐1246 was higher in LSCC tissues and plasma sEV. MiR‐1246 was enriched in sEV rather than soluble form. SEV could be internalized into adjacent cells. Lack of miR‐1246 in sEV abrogated the tumorigenesis of LSCC. Furthermore, CCNG2 knockdown arrested the cell cycle and correlated to clinicopathological features and prognosis of LSCC patients. Taken together, we found that the function of sEV miR‐1246 by regulating CCNG2 is responsible for LSCC advancement with emphasis on the main source of miR‐1246 mainly root in sEV rather than in soluble form.

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RETRACTED: MicroRNA-1246 inhibits cell invasion and epithelial mesenchymal transition process by targeting CXCR4 in lung cancer cells

Abstract: These results demonstrated that miR-1246 inhibited cell invasion and EMT process by targeting CXCR4 and blocking JAK/STAT and PI3K/AKT signal pathways in lung cancer cells.

Cited by 39 publications

References 31 publications

<p>MicroRNA-1246 Promotes Melanoma Progression Through Targeting FOXA2</p>

<p>MicroRNA-1246 Promotes Melanoma Progression Through Targeting FOXA2</p>

lncRNA MIAT suppression alleviates corneal angiogenesis through regulating miR-1246/ACE

Lack of miR‐1246 in small extracellular vesicle blunts tumorigenesis of laryngeal carcinoma cells by regulating Cyclin G2

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