The non-coding RNA of the multidrug resistance-linked vault particle encodes multiple regulatory small RNAs

Persson, Helena; Kvist, Anders; Vallon‐Christersson, Johan; Medstrand, Patrik; Borg, Åke; Rovira, Carlos

doi:10.1038/ncb1972

Cited by 156 publications

(183 citation statements)

References 18 publications

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“…Thus, they are both characterized by the same recurrent t(6;9) translocation resulting in the MYB-NFIB gene fusion. 31,85 Overexpression of the MYB oncogene is a hallmark of adenoid cystic carcinoma irrespective of anatomical location. 32,85,86 Despite these similarities, there are important differences between these tumors.…”

Section: Discussionmentioning

confidence: 99%

“…30,31 Briefly, tumor tissue was minced into small pieces and digested in a collagenase solution (1000 U collagenase/ml) (Sigma-Aldrich) for 60 min at room temperature. The tumor cell suspension was washed twice in culture medium and seeded out in 25 cm 2 flasks.…”

Section: Cell Culturementioning

confidence: 99%

“…31 DNase treated (DNA-freeTM; Ambion, Austin, TX, USA) total RNA was subsequently converted to cDNA using the SuperScriptTM FirstStrand Synthesis System according to the manufacturer's manual (Invitrogen). The MYB-NFIB fusion transcripts were amplified by PCR using previously published primer sets.…”

Section: Myb-nfib Fusion Gene Screeningmentioning

confidence: 99%

“…The MYB-NFIB fusion transcripts were amplified by PCR using previously published primer sets. 31,32 PCR products were gel-purified and sequenced using an ABI PRISM 310 Genetic Analyzer (Applied Biosystems, Foster City, CA, USA).…”

Section: Myb-nfib Fusion Gene Screeningmentioning

confidence: 99%

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K5/K14-positive cells contribute to salivary gland-like breast tumors with myoepithelial differentiation

et al. 2013

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Salivary gland-like tumors of the breast show a great variety of architectural patterns and cellular differentiations such as glandular, myoepithelial, squamous, and even mesenchymal phenotypes. However, currently little is known about the evolution and cellular differentiation of these tumors. For that reason, we performed an in situ triple immunofluorescence lineage/differentiation tracing (isTILT) and qRT-PCR study of basal (K5/K14), glandular (K7/K8/18), and epidermal-specific squamous (K10) keratins, p63, and smooth muscle actin (SMA; myoepithelial marker) with the aim to construct and trace different cell lineages and define their cellular hierarchy in tumors with myoepithelial differentiation. isTILT analysis of a series of 28 breast, salivary, and lacrimal gland tumors, including pleomorphic adenomas (n ¼ 8), epithelial-myoepithelial tumors (n ¼ 9), and adenoid cystic carcinomas (n ¼ 11) revealed that all tumor types contained K5/K14-positive progenitor cells in varying frequencies from a few percent up to 15%. These K5/K14-positive tumor cells were found to differentiate to glandular-(K8/18-positive) and myoepithelial-lineage (SMA-positive)-specific cells and were also shown to generate various heterologeous cell differentiations such as squamous and mesenchymal progenies. p63 was co-expressed with K5/K14 in basal-like progenitor cells, myoepithelial, and squamous cells but not in glandular cells. Our results show that the corresponding counterpart tumors of breast and salivary/lacrimal glands have identical cellular compositions. Taken together, our isTILT and RNA-expression data indicate that look-alike tumors of the breast represent a special subgroup of basal-type tumors with benign or usually low malignant potential.

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Section: Discussionmentioning

confidence: 99%

Section: Cell Culturementioning

confidence: 99%

Section: Myb-nfib Fusion Gene Screeningmentioning

confidence: 99%

Section: Myb-nfib Fusion Gene Screeningmentioning

confidence: 99%

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K5/K14-positive cells contribute to salivary gland-like breast tumors with myoepithelial differentiation

et al. 2013

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“…Despite this lack of knowledge, the observation that ncRNAs can regulate the tumor response to different therapeutic drugs revealed their importance not only as biomarkers but also as potential therapeutic targets (Persson et al, 2009). As an example, the overexpression of the long ncRNA PCGEM1 (prostate cancer gene expression marker 1) in prostate cancer models confers resistance against sodium selenite and doxorubicin, thus supporting the escape of prostate cancer cells from drug-induced apoptosis (Srikantan et al, 2000).…”

Section: Novel Paradigms For Cancer Therapy V Pavet Et Almentioning

confidence: 99%

Towards novel paradigms for cancer therapy

et al. 2010

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Cancer is a complex progressive multistep disorder that results from the accumulation of genetic and epigenetic abnormalities, which lead to the transformation of normal cells into malignant derivatives. Despite enormous progress in the understanding of cancer biology including the decryption of multiple regulatory networks governing cell growth and death, and despite the possibility of analyzing (epi)genetic deregulation at the genome-wide scale, cancertargeted therapy is still the exception. In fact, to date there are still far too few examples of therapies leading to cure; treatment-derived toxicity is a major issue, and cancer remains to be one of the largest causes of death worldwide. The purpose of this review is to discuss the state of the art of cancer therapy with respect to the key issue of any treatment, namely its target selectivity. Therefore, we recapitulate and discuss current concepts and therapies targeting tumorspecific features, including oncofusion proteins, aberrant kinase activities and epigenetic tumor makeup. We analyze strategies designed to induce tumor-selective death such as the use of oncolytic virus, tumoricidal proteins (NS1, Eorf4, apoptin, HAMLET (human a-lactalbumin made lethal to tumor cells)) and activation of signaling pathways involved in tumor surveillance. We emphasize the potential of the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) pathway, an essential component of the evolutionary developed defense systems that eradicate malignant cells. Finally, we discuss the necessity of targeting tumor-initiating cells (TICs) to avoid relapse and increase the chances of complete remission, and describe emerging concepts that might provide novel avenues for cancer therapy.

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Evolution of VaultRNAs

Mosig

Stadler

2011

Encyclopedia of Life Sciences

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Vault ribonucleic acids (RNAs) are small, about 100 nt long, polymerase transcripts contained in the vault particles of eukaryotic cells. Although vaults are present in many but by no means all eukaryotes, an RNA component has been described in metazoa only. The RNAs exhibit conserved regions at the 3′ and 5′ ends containing also internal promoter elements. They form a panhandle‐like well‐conserved secondary structure. Most genomes contain only one or a small number of closely related vault RNA sequences. Only eutheria exhibit two clearly distinguished paralogues at syntenically conserved genomic locations. Their phylogenetic distribution is characterised by losses in major clades, whereas lophotrochozoa have vault particles and vault RNAs, and the entire system has been deleted in all ecdysozoa. Key Concepts: Vault RNA can be traced evolutionarily along with the vault particle and its key protein components, most notably MVP . Vault RNA exhibits a concserved pan‐handle secondary structure and expression patterns that are often mistaken as a microRNA.

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The non-coding RNA of the multidrug resistance-linked vault particle encodes multiple regulatory small RNAs

Cited by 156 publications

References 18 publications

K5/K14-positive cells contribute to salivary gland-like breast tumors with myoepithelial differentiation

K5/K14-positive cells contribute to salivary gland-like breast tumors with myoepithelial differentiation

Towards novel paradigms for cancer therapy

Evolution of VaultRNAs

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