MicroRNA-374a activates Wnt/β-catenin signaling to promote breast cancer metastasis

Cai, Junchao; Guan, Hongyu; Fang, Lishan; Yang, Yi; Zhu, Xun; Yuan, Jie; Wu, Jueheng; Li, Mengfeng

doi:10.1172/jci65871

Cited by 262 publications

(308 citation statements)

References 56 publications

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“…Wnt signalling pathway has been shown to control self-renewal and differentiation of cancer cells 29 , and aberrant activation of Wnt signalling leads to EMT in breast epithelial cells 41,42 . As a receptor for the Wnt pathway, FZD10 is expressed at high level in colorectal cancers, gastric cancers, as well as in synovial sarcomas, and is associated with the activation of Wnt signalling in these cancers 33,34,43 .…”

Section: Discussionmentioning

confidence: 99%

BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10

Gong

et al. 2014

Nat Commun

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BRMS1L (breast cancer metastasis suppressor 1 like, BRMS1-like) is a component of Sin3A-histone deacetylase (HDAC) co-repressor complex that suppresses target gene transcription. Here we show that reduced BRMS1L in breast cancer tissues is associated with metastasis and poor patient survival. Functionally, BRMS1L inhibits breast cancer cells migration and invasion by inhibiting epithelial-mesenchymal transition. These effects are mediated by epigenetic silencing of FZD10, a receptor for Wnt signalling, through HDAC1 recruitment and histone H3K9 deacetylation at the promoter. Consequently, BRMS1L-induced FZD10 silencing inhibits aberrant activation of WNT3-FZD10-b-catenin signalling. Furthermore, BRMS1L is a target of miR-106b and miR-106b upregulation leads to BRMS1L reduction in breast cancer cells. RNA interference-mediated silencing of BRMS1L expression promotes metastasis of breast cancer xenografts in immunocompromised mice, whereas ectopic BRMS1L expression inhibits metastasis. Therefore, BRMS1L provides an epigenetic regulation of Wnt signalling in breast cancer cells and acts as a breast cancer metastasis suppressor.

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Section: Discussionmentioning

confidence: 99%

BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10

Gong

et al. 2014

Nat Commun

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“…Aberrant regulation of miRNAs has been involved in a number of human diseases, including cancers. In tumorigenesis, miRNAs may act as tumor suppressors (5,6) or oncogenes (7,8) in different types of cancers, including esophageal cancer (9). Recent clinical findings indicated that the upregulation of miR-146b was associated with poor survival in esophageal squamous cell carcinoma (10).…”

Section: Introductionmentioning

confidence: 99%

“…miRNA profiling has shown that microRNA-374a (miR-374a) is overexpressed in many types of cancer, such as head and neck squamous cell carcinoma, follicular lymphoma, osteosarcoma and bladder urothelial carcinoma (15)(16)(17)(18). In breast cancer, miR-374a was markedly upregulated in primary tumor samples from patients with distant metastases and was considered to be associated with poor metastasis-free survival (7). In gefitinib-resistant lung cancer cells, the expression of miR-374a was high (19).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-374a promotes esophageal cancer cell proliferation via Axin2 suppression

et al. 2015

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Abstract. is involved in the progress of various types of cancer, and may indicate a poor prognosis. However, its role in esophageal cancer remains to be determined. In the present study, the role of miR-374a in esophageal cancers and cancer cell growth was examined using miR-374a overexpression and underexpression models. The results showed that miR-374a was markedly increased in esophageal cancer cell lines and tumor samples from patients with esophageal cancer. In esophageal cancer Eca109 cells, the ectopic overexpression of miR-374a promoted cell growth. Additionally, cell growth was reduced by miR-374a inhibition. The mechanisms underlying the promotive role were examined and it was found that miR-374a significantly decreased the expression and transcription activity of axis inhibition protein 2 (Axin2). Axin2, a tumor suppressor, exhibited a marked inhibitory effect on Eca109 cell growth. The results identified a new role of miR-374a in esophageal cancer involving Axin2 suppression.

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“…In this experiment the E-cadherin expression was up-regulated by nLQ, implicating that the EMT could be reversed by nLQ at certain extent. It is suggested that the reversal EMT induced by nLQ may inhibit cancer cell metastatic stemness potency via wnt/β-catenin pathway (Cai, et al, 2013). Almanaa TN et al indicate that the anti-stem like cell effects can be induced by phytochemical agent, curcumin, in human esophageal cancer cells (Almanaa et al, 2012), the apoptotic effect via HDAC-NF-κB cascade signaling induced by the phytochemical agent, quercetin, was studied in this experiment.…”

Section: Discussionmentioning

confidence: 88%

Anti-CSC Effects in Human Esophageal Squamous Cell Carcinomas and Eca109/9706 Cells Induced by Nanoliposomal Quercetin Alone or Combined with CD 133 Antiserum

Naigang¹,

Mo²,

Li³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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CD133 was recently reported to be a cancer stem cell and prognostic marker. Quercetin is considered as a potential chemopreventive agent due to its involvement in suppression of oxidative stress, proliferation and metastasis. In this study, the expression of CD133/CD44 in esophageal carcinomas and Eca109/9706 cells was explored. In immunoflurorescence the locations of CD133 + and multidrug resistance 1 (MDR 1) + in the same E-cancer cells were coincident, mainly in cytomembranes. In esophageal squamous cell carcinomas detected by double/single immunocytochemistry, small CD133 + cells were located in the basal layer of stratified squamous epithelium, determined as CSLC (cancer stem like cells); CD44 + surrounding the cells appeared in diffuse pattern, and the larger CD44 + (hi) cells were mainly located in the prickle cell layer of the epithelium, as progenitor cells. In E-cancer cells exposed to nanoliposomal quercetin (nLQ with cytomembrane permeability), down-regulation of NF-κBp65, histone deacetylase 1 (HDAC1) and cyclin D1 and up-regulation of caspase-3 were shown by immunoblotting, and attenuated HDAC1 with nuclear translocation and promoted E-cadherin expression were demonstrated by immunocytochemistry. In particular, enhanced E-cadherin expression reflected the reversed epithelial mesenchymal transition (EMT) capacity of nLQ, acting as cancer attenuator/preventive agent. nLQ acting as an HDAC inhibitor induced apoptotic cells detected by TUNEL assay mediated via HDAC-NF-κB signaling. Apoptotic effects of liposomal quercetin (LQ, with cytomembrane-philia) combined with CD133 antiserum were also detected by CD133 immunocytochemistry combined with TUNEL assay. The combination could induce greater apoptotic effects than nLQ induced alone, suggesting a novel anti-CSC treatment strategy.

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MicroRNA-374a activates Wnt/β-catenin signaling to promote breast cancer metastasis

Cited by 262 publications

References 56 publications

BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10

BRMS1L suppresses breast cancer metastasis by inducing epigenetic silence of FZD10

MicroRNA-374a promotes esophageal cancer cell proliferation via Axin2 suppression

Anti-CSC Effects in Human Esophageal Squamous Cell Carcinomas and Eca109/9706 Cells Induced by Nanoliposomal Quercetin Alone or Combined with CD 133 Antiserum

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