Competing Endogenous RNA and Interactome Bioinformatic Analyses on Human Telomerase

Arancio, Walter; Pizzolanti, Giuseppe; Genovese, Swonild Ilenia; Baiamonte, Concetta; Giordano, Carla

doi:10.1089/rej.2013.1486

Cited by 26 publications

(27 citation statements)

References 27 publications

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“…The upregulation of one transcript causes more copies of the shared miRNA to be sequestrated and thus the de-repression of the other transcript, and vice versa. However, in the real cellular context, this oversimplified ‘one-to-one’ model is replaced by ‘multiple-to-multiple’ ceRNA interactions that constitute a complex regulatory network 11 12…”

Section: Mechanisms and Molecular Bases Of Cerna Interplaymentioning

confidence: 99%

ceRNA in cancer: possible functions and clinical implications

et al. 2015

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Competing endogenous RNAs (ceRNAs) are transcripts that can regulate each other at post-transcription level by competing for shared miRNAs. CeRNA networks link the function of protein-coding mRNAs with that of non-coding RNAs such as microRNA, long non-coding RNA, pseudogenic RNA and circular RNA. Given that any transcripts harbouring miRNA response element can theoretically function as ceRNAs, they may represent a widespread form of post-transcriptional regulation of gene expression in both physiology and pathology. CeRNA activity is influenced by multiple factors such as the abundance and subcellular localisation of ceRNA components, binding affinity of miRNAs to their sponges, RNA editing, RNA secondary structures and RNA-binding proteins. Aberrations in these factors may deregulate ceRNA networks and thus lead to human diseases including cancer. In this review, we introduce the mechanisms and molecular bases of ceRNA networks, discuss their roles in the pathogenesis of cancer as well as methods of predicting and validating ceRNA interplay. At last, we discuss the limitations of current ceRNA theory, propose possible directions and envision the possibilities of ceRNAs as diagnostic biomarkers or therapeutic targets.

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Section: Mechanisms and Molecular Bases Of Cerna Interplaymentioning

confidence: 99%

ceRNA in cancer: possible functions and clinical implications

et al. 2015

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“…Several studies indicated that some specific lncRNAs can function as miRNA sponges to control miRNAs available for binding to their targets, functionally liberating mRNA transcripts targeted by certain miRNAs. 13,14 This function introduces an extra layer of complexity in the miRNA-target interaction network. 15 Previously, Liao et al 16 reported that lncRNA CASC2 interacts with miR-181a to modulate BC growth and resistance to TMZ through PTEN pathway.…”

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confidence: 99%

TP73‐AS1 promotes breast cancer cell proliferation through miR‐200a‐mediated TFAM inhibition

Yao

Zhang

et al. 2017

J of Cellular Biochemistry

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P73 antisense RNA 1T (TP73-AS1 or PDAM) is a long non-coding RNA, which can regulate apoptosis through regulation of p53 signaling-related anti-apoptotic genes. An abnormal change of TP73-AS1 expression was noticed in cancers. The effects of TP73-AS1 in breast cancer (BC) growth and the underlying mechanism remain unclear so far. In the present study, the effect of TP73-AS1 in BC cell lines and clinical tumor samples was detected so as to reveal its role and function. In the present study, TP73-AS1 was specifically upregulated in BC tissues and BC cell lines and was correlated to a poorer prognosis in patients with BC. TP73-AS1 knocking down

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“…Different patterns of hTERT transcription are required for functions as different as tissue renewal, differentiation, immune cell proliferation and tumor prevention. Accordingly, a complex network of regulatory gene products, signaling pathways and expression overrides is required for hTERT to accommodate its diverse range of responses to a vast range of environmental input [8, 10-12]. Regulation of the cell cycle, cross-linked to regulation of hTERT expression as has been noted [8, 13-14], controls a wide range of bodily functions and development [8-12, 15], and dysregulation accommodates a wide range of human diseases.…”

Section: Introductionmentioning

confidence: 99%

“…Accordingly, a complex network of regulatory gene products, signaling pathways and expression overrides is required for hTERT to accommodate its diverse range of responses to a vast range of environmental input [8, 10-12]. Regulation of the cell cycle, cross-linked to regulation of hTERT expression as has been noted [8, 13-14], controls a wide range of bodily functions and development [8-12, 15], and dysregulation accommodates a wide range of human diseases. hTERT is especially valuable as a target for prevention or treatment of the unlimited cell cycle progression, immortality, that sustains cancer [2, 4-5].…”

Section: Introductionmentioning

confidence: 99%

Down-regulation of hTERT and Cyclin D1 transcription via PI3K/Akt and TGF-β pathways in MCF-7 Cancer cells with PX-866 and Raloxifene

Peek

Tollefsbol

2016

Experimental Cell Research

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Human telomerase reverse transcriptase (hTERT) is the catalytic and limiting component of telomerase and also a transcription factor. It is critical to the integrity of the ends of linear chromosomes and to the regulation, extent and rate of cell cycle progression in multicellular eukaryotes. The level of hTERT expression is essential to a wide range of bodily functions and to avoidance of disease conditions, such as cancer, that are mediated in part by aberrant level and regulation of cell cycle proliferation. Value of a gene in regulation depends on its ability to both receive input from multiple sources and transmit signals to multiple effectors. The expression of hTERT and the progression of the cell cycle have been shown to be regulated by an extensive network of gene products and signaling pathways, including the PI3K/Akt and TGF-β pathways. The PI3K inhibitor PX-866 and the competitive estrogen receptor ligand raloxifene have been shown to modify progression of those pathways and, in combination, to decrease proliferation of estrogen receptor positive (ER+) MCF-7 breast cancer cells. We found that combinations of modulators of those pathways decreased not only hTERT transcription but also transcription of additional essential cell cycle regulators such as Cyclin D1. By evaluating known expression profile signatures for TGF-β pathway diversions, we confirmed additional genes such as heparin-binding epidermal growth factor-like growth factor (HB EGF) by which those pathways and their perturbations may also modify cell cycle progression.

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Competing Endogenous RNA and Interactome Bioinformatic Analyses on Human Telomerase

Cited by 26 publications

References 27 publications

ceRNA in cancer: possible functions and clinical implications

ceRNA in cancer: possible functions and clinical implications

TP73‐AS1 promotes breast cancer cell proliferation through miR‐200a‐mediated TFAM inhibition

Down-regulation of hTERT and Cyclin D1 transcription via PI3K/Akt and TGF-β pathways in MCF-7 Cancer cells with PX-866 and Raloxifene

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