The Noncoding RNA Revolution—Trashing Old Rules to Forge New Ones

Cech, Thomas R.; Steitz, Joan A.

doi:10.1016/j.cell.2014.03.008

Cited by 2,079 publications

(1,602 citation statements)

References 209 publications

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“…More recently, we have come to learn that here too small RNA's (such as CRISPRS or even tRNAs) are much more involved in basic regulatory functions (Nicolas et al 2013. And in eukaryotes, there has been a big change in our thinking regarding regulation by RNA (Cech and Steitz 2014). Thus, we propose to place RNA-based regulation in a more fundamental role (Supplementary File 3).…”

Section: The Basic Motif: Virus-derived Addiction Modules Promote Gromentioning

confidence: 99%

When Competing Viruses Unify: Evolution, Conservation, and Plasticity of Genetic Identities

Villarreal

Witzany

2015

J Mol Evol

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In the early 1970s, Manfred Eigen and colleagues developed the quasispecies model (qs) for the population-based origin of RNAs representing the early genetic code. The Eigen idea is basically that a halo of mutants is generated by error-prone replication around the master fittest type which will behave similarly as a biological population. But almost from the start, very interesting and unexpected observations were made regarding competition versus co-operation which suggested more complex interactions. It thus became increasingly clear that although viruses functioned similar to biological species, their behavior was much more complex than the original theory could explain, especially adaptation without changing the consensus involving minority populations. With respect to the origin of natural codes, meaning, and code-use in interactions (communication), it also became clear that individual fittest type-based mechanisms were likewise unable to explain the origin of natural codes such as the genetic code with their context-and consortia-dependence (pragmatic nature). This, instead, required the participation of groups of agents competent in the code and able to edit code because natural codes do not code themselves. Three lines of inquiry, experimental virology, quasispecies theory, and the study of natural codes converged to indicate that consortia of cooperative RNA agents such as viruses must be involved in the fitness of RNA and its involvement in communication, i.e., code-competent interactions. We called this co-operative form quasispecies consortia (qs-c). They are the essential agents that constitute the possibility of evolution of biological group identity. Finally, the basic interactional motifs for the emergence of group identity, communication, and cooperation-together with its opposing functions-are explained by the ''Gangen'' hypothesis.

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Section: The Basic Motif: Virus-derived Addiction Modules Promote Gromentioning

confidence: 99%

When Competing Viruses Unify: Evolution, Conservation, and Plasticity of Genetic Identities

Villarreal

Witzany

2015

J Mol Evol

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“…The lncRNAs work in a complicated way as critical regulator of epigenetic modulation, transcription and translation in a spatiotemporal manner 13, 14. SNHG14, alternatively named UBE3A‐ATS, is located on chromosome 15q11.2.…”

Section: Introductionmentioning

confidence: 99%

Long non‐coding RNA SNHG14 induces trastuzumab resistance of breast cancer via regulating PABPC1 expression through H3K27 acetylation

Huang

Wang

et al. 2018

J Cellular Molecular Medi

100

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Currently, resistance to trastuzumab, a human epidermal growth factor receptor 2 (HER2) inhibitor, has become one major obstacle for improving the clinical outcome of patients with advanced HER2+ breast cancer. While cell behaviour can be modulated by long non‐coding RNAs (lncRNAs), the contributions of lncRNAs in progression and trastuzumab resistance of breast cancer are largely unknown. To this end, the involvement and regulatory functions of lncRNA SNHG14 in human breast cancer were investigated. RT‐qPCR assay showed that SNHG14 was up‐regulated in breast cancer tissues and associated with trastuzumab response. Gain‐ and loss‐of‐function experiments revealed that overexpression of SNHG14 promotes cell proliferation, invasion and trastuzumab resistance, whereas knockdown of SNHG14 showed an opposite effect. PABPC1 gene was identified as a downstream target of SNHG14, and PABPC1 mediates the SNHG14‐induced oncogenic effects. More importantly, ChIP assays demonstrated that lncRNA SNHG14 may induce PABPC1 expression through modulating H3K27 acetylation in the promoter of PABPC1 gene, thus resulting in the activation of Nrf2 signalling pathway. These data suggest that lncRNA SNHG14 promotes breast cancer tumorigenesis and trastuzumab resistance through regulating PABPC1 expression through H3K27 acetylation. Therefore, SNHG14 may serve as a novel diagnostic and therapeutic target for breast cancer patients.

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“…long noncoding RNAs (lncRNAs) are the new member of ncRNA with a length >200 nt, and lacking of protein‐coding capacity 9. To date, increasing evidence have demonstrated that lncRNAs are widely expressed in most of organ tissues, and participate in various cellular biological process, including X chromatin imprinting, muscle cells differentiation, immune response, cell fate decision, tumor cell proliferation, and drug resistance 10, 11. Importantly, RNA sequencing and microarray analyses of tumor and normal tissues in diverse types of human cancers revealed that thousands of lncRNAs are dysregulated in cancer tissues, and part of these lncRNAs are emerging as key molecules during carcinogenesis 12, 13.…”

Section: Introductionmentioning

confidence: 99%

A genome‐wide analysis of long noncoding RNA profile identifies differentially expressed lncRNAs associated with Esophageal cancer

et al. 2018

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Esophageal cancer is one of the most common cancers and a leading cause of cancer‐related death worldwide. However, the mechanism of esophageal cancer pathogenesis remains poorly understood. Long noncoding RNAs (lncRNAs) dysregulation have been reported to involve in various human cancers, which highlights the potential of lncRNAs used as novel biomarkers for cancer diagnosis. Although more efforts have been made to identify novel lncRNAs signature in esophageal cancer, the expression pattern, prognostic value, and biological function of most lncRNAs in esophageal cancer still need to be systematically investigated. In this study, we comprehensively analyzed the expression profile of lncRNAs in more than 200 esophageal cancer patients tissue samples from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO). We identified thousands of lncRNAs are differentially expressed in esophageal cancer tissues, and many of those lncRNAs expression are associated with patients overall survival or recurrence‐free survival time. Moreover, copy number variation analyses revealed that genomic loci copy number amplification or deletion might contribute to these lncRNAs dysregulation. Among these lncRNAs, DUXAP8 and LINC00460 were significantly upregulated, and GO enrichment analyses indicated that the two lncRNAs associated protein‐coding genes involve with many known biological processes, such as cell cycle and cell‐cell adherens junction. Further experimental validation revealed that knockdown of DUXAP8 could impair esophageal cancer cells proliferation and invasion in vitro. Taken together, our findings identified more aberrantly expressed lncRNAs in esophageal cancer that may provide a useful resource for identifying novel esophageal cancer associated lncRNAs.

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The Noncoding RNA Revolution—Trashing Old Rules to Forge New Ones

Cited by 2,079 publications

References 209 publications

When Competing Viruses Unify: Evolution, Conservation, and Plasticity of Genetic Identities

When Competing Viruses Unify: Evolution, Conservation, and Plasticity of Genetic Identities

Long non‐coding RNA SNHG14 induces trastuzumab resistance of breast cancer via regulating PABPC1 expression through H3K27 acetylation

A genome‐wide analysis of long noncoding RNA profile identifies differentially expressed lncRNAs associated with Esophageal cancer

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