Down-regulation of miR-30a-3p/5p promotes esophageal squamous cell carcinoma cell proliferation by activating the Wnt signaling pathway

Qi, Bo; Wang, Yan; Chen, Zhijun; Li, Xiangnan; Qi, Yu; Yang, Yang; Cui, Guanghui; Guo, Haizhou; Li, Weihao; Zhao, Song

doi:10.3748/wjg.v23.i45.7965

Cited by 52 publications

(38 citation statements)

References 48 publications

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“…EC is one of the most common types of cancer accompanied by poor prognosis, and the poor outcomes in EC patients are related to diagnosis at advanced stages and the tendency for metastases (Liu et al ., ). lncRNAs and miRNAs have been revealed to have the potential to function in the initiation and progression of EC (Pan et al ., ; Qi et al ., ). The present study explored the mechanism of how lncRNA PVT1 and miR‐145 function in EC cells.…”

Section: Discussionmentioning

confidence: 97%

Retracted: Down‐regulation of long noncoding RNA PVT1 inhibits esophageal carcinoma cell migration and invasion and promotes cell apoptosis via microRNA‐145‐mediated inhibition of FSCN1

Shen

Liu

et al. 2019

Molecular Oncology

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Accumulating evidence has established that long noncoding RNA (lncRNA) plasmacytoma variant translocation 1 (PVT1) is a tumor regulator in many cancers. Here, we aimed to investigate the possible function of lncRNA PVT1 in esophageal carcinoma (EC) via targeting of microRNA‐145 (miR‐145). Initially, microarray‐based gene expression profiling of EC was employed to identify differentially expressed genes. Moreover, the expression of lncRNA PVT1 was examined and the cell line presenting with the highest level of lncRNA PVT1 expression was selected for subsequent experiments. We then proceeded to examine interaction among lncRNA PVT1, FSCN1, and miR‐145. The effect of lncRNA PVT1 on viability, migration, invasion, apoptosis, and tumorigenesis of transfected cells was examined with gain‐of‐function and loss‐of‐function experiments. We observed that lncRNA PVT1 was robustly induced in EC. lncRNA PVT1 could bind to miR‐145 and regulate its expression, and FSCN1 is a target gene of miR‐145. Overexpression of miR‐145 or silencing of lncRNA PVT1 was revealed to suppress cell viability, migration, and invasion abilities, while also stimulating cell apoptosis. Furthermore, our in vivo results showed that overexpression of miR‐145 or silencing of lncRNA PVT1 resulted in decreased tumor growth in nude mice. In conclusion, our research reveals that down‐regulation of lncRNA PVT1 could potentially promote expression of miR‐145 to repress cell migration and invasion, and promote cell apoptosis through the inhibition of FSCN1. This highlights the potential of lncRNA PVT1 as a therapeutic target for EC treatment.

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Section: Discussionmentioning

confidence: 97%

Retracted: Down‐regulation of long noncoding RNA PVT1 inhibits esophageal carcinoma cell migration and invasion and promotes cell apoptosis via microRNA‐145‐mediated inhibition of FSCN1

Shen

Liu

et al. 2019

Molecular Oncology

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“…Furthermore, mir29b-3p has been shown to act as a tumor suppressor in glioblastoma where it can inhibit cell growth and induce apoptosis in vitro [42] . In addition, a reciprocal correlation was found between miR-30a-3p expression and esophageal cancer cells proliferation [43] . This clearly underlines the cell type-specific effect of miRNAs despite the nature of the disease.…”

Section: Discussionmentioning

confidence: 88%

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Alwhaibi

Gao

Artham

et al. 2018

Heliyon

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Recent studies indicate a stage-specific, differential role for the oncogene Akt on various cancers. In prostate cancer (PCa), suppression of Akt activity in the advanced stages promoted transforming growth factor-β (TGFβ) pathway-mediated epithelial-to-mesenchymal transition (EMT) and metastasis to the lungs. In the current study, we performed Affymetrix analysis to compare the expression profile of microRNAs in the mouse prostate tissues collected at the prostatic inter-epithelial neoplasia (PIN) stage from Transgenic adenocarcinoma of the mouse (TRAMP)/Akt1+/+ versus TRAMP/Akt1–/– mice, and at the advanced stage from TRAMP/Akt1+/+ mice treated with triciribine (Akt inhibitor) versus DMSO-treated control. Our analysis demonstrates that in the early stage, Akt1 in the TRAMP prostate tumors express a set of miRNAs responsible for regulating cancer cell survival, proliferation, and tumor growth, whereas, in the advanced stages, a different set of miRNAs that promote EMT and cancer metastasis is expressed. Our study has identified novel Akt-regulated signature microRNAs in the early and advanced PCa and demonstrates their differential effects on PCa growth and metastasis.

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“…As a result, β-catenin is recognized by β-Trcp and the sub-unit of E3 ubiquitin ligases and is then degraded by the ubiquitination pathway. The continuous removal of β-catenin inhibits the nuclear import of β-catenin and the combination of the protein family of T cell factor/lymphoid enhancer factor (TCF/LEF) with DNA, thus suppressing the transcription of Wnt target genes[ 21 , 22 ]. When Wnt ligands are bound with transmembrane Frizzled (Fz) receptors and their co-receptor–low-density lipoprotein receptor related protein 6 (LRP6) or similar LRP5, the Wnt/β-catenin signalling pathway and dishevelled Dsh/Dvl proteins in cells are activated.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of combined use of vitamin D and puerarin in anti-hepatic fibrosis by regulating the Wnt/β-catenin signalling pathway

Huang¹,

Wei²,

Huang³

et al. 2018

WJG

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AIMTo reveal the protective mechanism of the combined use of vitamin D and puerarin in the progression of hepatic fibrosis induced by carbon tetrachloride (CCl4).METHODSEight-week-old male Wistar rats were randomly divided into a normal control group (C group), a CCl4 group (CCl4 group), a vitamin D group (V group), a puerarin group (P group), and a combined group of vitamin D and puerarin (V + P group), each of which contained ten rats. In this way, we built a rat model of CCl4-induced hepatic fibrosis with intervention by vitamin D, puerarin, or a combination of the two. After eight weeks, the mice were sacrificed to collect serum and liver specimens. Blood was collected to detect the hyaluronic acid (HA). We also measured hydroxyproline (Hyp) and prepared paraffin sections of liver. After Sirius red staining, the liver specimens were observed under a microscope. RT-PCR and western blot analysis were adopted to detect the mRNA and the protein levels of Collagen I, Collagen III, Wnt1, and β-catenin in the liver tissues, respectively.RESULTSHepatic fibrosis was observed in the CCl4 group. In comparison, hepatic fibrosis was attenuated in the V, P, and V + P groups: the HA level in blood and the Hyp level in liver were reduced, and the mRNA levels of Collagen I, Collagen III, Wnt, and β-catenin in liver were also decreased, as well as the protein levels of Wnt1 and β-catenin. Among these groups, the V + P group demonstrated the greatest amelioration of hepatic fibrosis.CONCLUSIONThe combined application of vitamin D and puerarin is capable of alleviating CCl4-induced hepatic fibrosis of rats. As to the mechanism, it is probably because the combined use is able to silence the Wnt1/β-catenin pathway, suppress the activation of hepatic stellate cells, and reduce the secretion of collagen fibers, therefore improving the anti-hepatic fibrosis effect.

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Down-regulation of miR-30a-3p/5p promotes esophageal squamous cell carcinoma cell proliferation by activating the Wnt signaling pathway

Cited by 52 publications

References 48 publications

Retracted: Down‐regulation of long noncoding RNA PVT1 inhibits esophageal carcinoma cell migration and invasion and promotes cell apoptosis via microRNA‐145‐mediated inhibition of FSCN1

Retracted: Down‐regulation of long noncoding RNA PVT1 inhibits esophageal carcinoma cell migration and invasion and promotes cell apoptosis via microRNA‐145‐mediated inhibition of FSCN1

Modulation in the microRNA repertoire is responsible for the stage-specific effects of Akt suppression on murine neuroendocrine prostate cancer

Mechanism of combined use of vitamin D and puerarin in anti-hepatic fibrosis by regulating the Wnt/β-catenin signalling pathway

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