The emerging role of exosome-derived non-coding RNAs in cancer biology

Fan, Qing; Yang, Liang; Zhang, Xiaodong; Peng, Xueqiang; Wei, Shibo; Su, Dongming; Zhai, Zhenhua; Hua, Xiangdong; Li, Hangyu

doi:10.1016/j.canlet.2017.10.040

Cited by 189 publications

(145 citation statements)

References 103 publications

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“…Functions of lncRNAs are associated with their subcellular fates. Web servers can assist in quickly assessing experimentally determined or predictive RNA-RNA interactions [204] or even RNA-protein interactions [205,206]. Depending on the subcellular or extracellular compartmental localization of a lncRNA, this patterning will elude to the regulatory role of the gene, as well as how a lncRNA might execute its function [207][208][209].…”

Section: Subcellular Localization and Binding Partnersmentioning

confidence: 99%

The how and why of lncRNA function: An innate immune perspective

Robinson

Covarrubias

2020

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

237

192

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Section: Subcellular Localization and Binding Partnersmentioning

confidence: 99%

The how and why of lncRNA function: An innate immune perspective

Robinson

Covarrubias

2020

Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanism

237

192

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“…Besides loading with proteins, the recruitment of miRNA and lncRNA has been extensively explored and is well-summarized in recent reviews (Hewson and Morris, 2016; Bortoluzzi et al, 2017; Fan et al, 2018; Salehi and Sharifi, 2018), some miRNA being preferentially recruited via CD44v6 (accession No: http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE34739, ENA database, accession No: PRJEB25446). Thus, non-stochastic miRNA-loading into tetraspanin-positive ILV proceeds preferentially via a ceramide-dependent pathway.…”

Section: Cic Cd44 and Texmentioning

confidence: 99%

CD44/CD44v6 a Reliable Companion in Cancer-Initiating Cell Maintenance and Tumor Progression

Wang

Zhao

Hackert

et al. 2018

Front. Cell Dev. Biol.

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Metastasis is the leading cause of cancer death, tumor progression proceeding through emigration from the primary tumor, gaining access to the circulation, leaving the circulation, settling in distant organs and growing in the foreign environment. The capacity of a tumor to metastasize relies on a small subpopulation of cells in the primary tumor, so called cancer-initiating cells (CIC). CIC are characterized by sets of markers, mostly membrane anchored adhesion molecules, CD44v6 being the most frequently recovered marker. Knockdown and knockout models accompanied by loss of tumor progression despite unaltered primary tumor growth unraveled that these markers are indispensable for CIC. The unexpected contribution of marker molecules to CIC-related activities prompted research on underlying molecular mechanisms. This review outlines the contribution of CD44, particularly CD44v6 to CIC activities. A first focus is given to the impact of CD44/CD44v6 to inherent CIC features, including the crosstalk with the niche, apoptosis-resistance, and epithelial mesenchymal transition. Following the steps of the metastatic cascade, we report on supporting activities of CD44/CD44v6 in migration and invasion. These CD44/CD44v6 activities rely on the association with membrane-integrated and cytosolic signaling molecules and proteases and transcriptional regulation. They are not restricted to, but most pronounced in CIC and are tightly regulated by feedback loops. Finally, we discuss on the engagement of CD44/CD44v6 in exosome biogenesis, loading and delivery. exosomes being the main acteurs in the long-distance crosstalk of CIC with the host. In brief, by supporting the communication with the niche and promoting apoptosis resistance CD44/CD44v6 plays an important role in CIC maintenance. The multifaceted interplay between CD44/CD44v6, signal transducing molecules and proteases facilitates the metastasizing tumor cell journey through the body. By its engagement in exosome biogenesis CD44/CD44v6 contributes to disseminated tumor cell settlement and growth in distant organs. Thus, CD44/CD44v6 likely is the most central CIC biomarker.

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“…5 Concurrently, lncRNAs play act as regulators in the occurrence and progress of cancers, and function either as an oncogene or as a tumor-suppressor gene by regulating tumor-related genes or pathways. 6,7 Till date, several cancer-related lncRNAs have been implicated in RB progression, and act as diagnostic markers and therapeutic target for RB. [8][9][10] A nuclear-restricted lncRNA, nuclear paraspeckle assembly transcript 1 (NEAT1), encodes two transcriptional variants, NEAT1-1 and NEAT1-2, of lengths 3756 and 22 743 bp, respectively.…”

Section: Introductionmentioning

confidence: 99%

NEAT1 promotes retinoblastoma progression via modulating miR‐124

Wang

Yang

Tian

et al. 2019

J of Cellular Biochemistry

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The long noncoding RNA nuclear‐enriched abundant transcript 1 (NEAT1) is reportedly involved in the initiation and progression of cancers of several types. However, the role, expression status, and the detailed mechanism of NEAT1 in retinoblastoma (RB) yet need to be unraveled. We explored the role and the mechanism of NEAT1 activity in RB. Our data show enhanced NEAT1 expression in RB‐affected tissues compared with the corresponding control. Functional experiments reveal that a NEAT1 knockdown in RB cells significantly inhibits proliferation, cycle progression, and facilitates apoptosis and caspase‐3 and ‐9 activities. Besides that, miR‐124 was predicted to be a target of NEAT1 and its reduced expression, as well as the inverse correlation of NEAT1 with miR‐124, was observed in RB‐affected tissues. Further, luciferase and RNA immunoprecipitation (RIP) assays confirmed the interaction between NEAT1 and miR‐124. Rescue experiments confirmed that the inhibition of miR‐124 could reverse the effect of NEAT1 on RB cell proliferation, cycle arrest, apoptosis, and caspase‐3 and ‐9 activities. Thus, NEAT1 promotes RB progression by sponging miR‐124, providing a therapeutic target for RB.

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The emerging role of exosome-derived non-coding RNAs in cancer biology

Cited by 189 publications

References 103 publications

The how and why of lncRNA function: An innate immune perspective

The how and why of lncRNA function: An innate immune perspective

CD44/CD44v6 a Reliable Companion in Cancer-Initiating Cell Maintenance and Tumor Progression

NEAT1 promotes retinoblastoma progression via modulating miR‐124

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