CXCR4 3′UTR functions as a ceRNA in promoting metastasis, proliferation and survival of MCF-7 cells by regulating miR-146a activity

Zheng, Tianjing; Chou, Jinjiang; Zhang, Feng; Liu, Yu; Ni, Haiwei; Li, Xiaoman; Zheng, Lufeng; Tang, Tingting; Jin, Liang; Xi, Tao

doi:10.1016/j.ejcb.2015.05.010

Cited by 27 publications

(24 citation statements)

References 48 publications

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“…ceRNAs have already been shown to play a role in critical cellular pathways. For example, our group has shown that 3 0 -UTRs of CDH5, HOXD1 and HOXD10 could inhibit breast cancer metastasis by serving as STARD13 ceRNAs [33] and CXCR4 could promote MCF-7 cells proliferation and metastasis by sequestering miR-146a and elevating the expression of other oncogenes [34]. In the present study, we overexpressed and knocked down the CYP4Z1-and CYP4Z2P-3 0 -UTR and detected apoptosis-related proteins, Bcl-2 and Bax.…”

Section: Discussionmentioning

confidence: 57%

The competing endogenousRNAnetwork ofCYP4Z1 and pseudogeneCYP4Z2P exerts an anti‐apoptotic function in breast cancer

Cheng

Zheng

et al. 2017

FEBS Letters

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The competing endogenous RNA network (ceRNET) is involved in tumorigenesis and has become a hot spot of research. The ceRNET between CYP4Z1 and the pseudogene CYP4Z2P promotes angiogenesis and mediates tamoxifen resistance in breast cancer. Nevertheless, the effects of this ceRNET on cell apoptosis and related mechanisms remain unclear. In the present study, we found that downregulation of CYP4Z1 or the CYP4Z2P 3'-UTR promotes cell apoptosis, mirroring the functions of human telomerase reverse transcriptase (hTERT). Furthermore, the ceRNET between CYP4Z1 and pseudogene CYP4Z2P modulates hTERT expression by operating as a sub-ceRNET for hTERT. Our data demonstrate that the ceRNET between CYP4Z1 and pseudogene CYP4Z2P acts as a sub-ceRNET for hTERT and, thus, inhibits breast cancer apoptosis.

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Section: Discussionmentioning

confidence: 57%

The competing endogenousRNAnetwork ofCYP4Z1 and pseudogeneCYP4Z2P exerts an anti‐apoptotic function in breast cancer

Cheng

Zheng

et al. 2017

FEBS Letters

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“…In this regards, CXCR4 is known as a stemness marker of breast tumor stem cells and its expression can play an important role in determining the self‐renewal and metastatic features of BC stem cells (Ablett, O'Brien, Sims, Farnie, & Clarke, ). TRAF6 and EGFR are activating mediators of the nuclear transcription factor‐κB (NF‐κB) signaling pathway (T. Zheng, Chou, et al, ), which plays a key role in proliferation, survival, and metastasis of cancer cells (Karin, ).…”

Section: Cerna Interplay In Bc Development and Pathogenesismentioning

confidence: 99%

Competing endogenous RNA (ceRNA) cross talk and language in ceRNA regulatory networks: A new look at hallmarks of breast cancer

Abdollahzadeh

Daraei

Mansoori

et al. 2018

Journal Cellular Physiology

231

185

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Breast cancer (BC) is the most frequently occurring malignancy in women worldwide. Despite the substantial advancement in understanding the molecular mechanisms and management of BC, it remains the leading cause of cancer death in women. One of the main reasons for this obstacle is that we have not been able to find the Achilles heel for the BC as a highly heterogeneous disease. Accumulating evidence has revealed that noncoding RNAs (ncRNAs), play key roles in the development of BC; however, the involving of complex regulatory interactions between the different varieties of ncRNAs in the development of this cancer has been poorly understood. In the recent years, the newly discovered mechanism in the RNA world is “competing endogenous RNA (ceRNA)” which proposes regulatory dialogues between different RNAs, including long ncRNAs (lncRNAs), microRNAs (miRNAs), transcribed pseudogenes, and circular RNAs (circRNAs). In the latest BC research, various studies have revealed that dysregulation of several ceRNA networks (ceRNETs) between these ncRNAs has fundamental roles in establishing the hallmarks of BC development. And it is thought that such a discovery could open a new window for a better understanding of the hidden aspects of breast tumors. Besides, it probably can provide new biomarkers and potential efficient therapeutic targets for BC. This review will discuss the existing body of knowledge regarding the key functions of ceRNETs and then highlights the emerging roles of some recently discovered ceRNETs in several hallmarks of BC. Moreover, we propose for the first time the “ceRnome” as a new term in the present article for RNA research.

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“…These manipulations also affected tumor cell growth rates, indicating potential in vivo effects of changes to mPR regulatory networks ( Sumazin et al, 2011 ). Since the publication of these three papers, numerous other examples of ceRNA regulation have been reported in muscle differentiation ( Cesana et al, 2011 ), human embryonic stem cell renewal ( Wang et al, 2013 ), regulation of sex determination by SRY ( Granados-Riveron and Aquino-Jarquin 2014 ), breast cancer ( Yang et al, 2014 ; Zheng et al, 2015a ; 2015b ), lymphoma ( Karreth et al, 2015 ) and the regulation of the tumor-related HMGA1 ( Esposito et al, 2014 ).…”

Section: Introductionmentioning

confidence: 99%

Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs

Phelps

Coss

Wang

et al. 2016

eLife

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The Reproducibility Project: Cancer Biology seeks to address growing concerns about reproducibility in scientific research by conducting replications of selected experiments from a number of high-profile papers in the field of cancer biology. The papers, which were published between 2010 and 2012, were selected on the basis of citations and Altmetric scores (Errington et al., 2014). This Registered Report describes the proposed replication plan of key experiments from “Coding-Independent Regulation of the Tumor Suppressor PTEN by Competing Endogenous 'mRNAs' by Tay and colleagues, published in Cell in 2011 (Tay et al., 2011). The experiments to be replicated are those reported in Figures 3C, 3D, 3G, 3H, 5A and 5B, and in Supplemental Figures 3A and B. Tay and colleagues proposed a new regulatory mechanism based on competing endogenous RNAs (ceRNAs), which regulate target genes by competitive binding of shared microRNAs. They test their model by identifying and confirming ceRNAs that target PTEN. In Figure 3A and B, they report that perturbing expression of putative PTEN ceRNAs affects expression of PTEN. This effect is dependent on functional microRNA machinery (Figure 3G and H), and affects the pathway downstream of PTEN itself (Figures 5A and B). The Reproducibility Project: Cancer Biology is a collaboration between the Center for Open Science and Science Exchange, and the results of the replications will be published by eLife.DOI: http://dx.doi.org/10.7554/eLife.12470.001

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CXCR4 3′UTR functions as a ceRNA in promoting metastasis, proliferation and survival of MCF-7 cells by regulating miR-146a activity

Cited by 27 publications

References 48 publications

The competing endogenousRNAnetwork ofCYP4Z1 and pseudogeneCYP4Z2P exerts an anti‐apoptotic function in breast cancer

The competing endogenousRNAnetwork ofCYP4Z1 and pseudogeneCYP4Z2P exerts an anti‐apoptotic function in breast cancer

Competing endogenous RNA (ceRNA) cross talk and language in ceRNA regulatory networks: A new look at hallmarks of breast cancer

Registered report: Coding-independent regulation of the tumor suppressor PTEN by competing endogenous mRNAs

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