A20 gene expression is regulated by TNF, Vitamin D and androgen in prostate cancer cells

Golovko, Olga; Nazarova, Nadja; Tuohimaa, Pentti

doi:10.1016/j.jsbmb.2005.01.019

Cited by 13 publications

(5 citation statements)

References 30 publications

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“…Each QD was conjugated to oligonucleotides complementary to either GAPDH (QD608), PTEN (QD693), or A20 (QD800) mRNA and were then mixed and applied simultaneously to LNCaP prostate cancer cells using the 1-step QD-FISH protocol. Expression levels were modulated by treating the cells with either anti- PTEN siRNA to knock down PTEN expression, or tumor necrosis factor alpha (TNF-α) to selectively induce A20 gene expression 22 , each validated by qRT-PCR in Fig. 4b .…”

Section: Resultsmentioning

confidence: 97%

Enhanced mRNA FISH with compact quantum dots

Liu

Lim

et al. 2018

Nat Commun

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Fluorescence in situ hybridization (FISH) is the primary technology used to image and count mRNA in single cells, but applications of the technique are limited by photophysical shortcomings of organic dyes. Inorganic quantum dots (QDs) can overcome these problems but years of development have not yielded viable QD-FISH probes. Here we report that macromolecular size thresholds limit mRNA labeling in cells, and that a new generation of compact QDs produces accurate mRNA counts. Compared with dyes, compact QD probes provide exceptional photostability and more robust transcript quantification due to enhanced brightness. New spectrally engineered QDs also allow quantification of multiple distinct mRNA transcripts at the single-molecule level in individual cells. We expect that QD-FISH will particularly benefit high-resolution gene expression studies in three dimensional biological specimens for which quantification and multiplexing are major challenges.

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Section: Resultsmentioning

confidence: 97%

Enhanced mRNA FISH with compact quantum dots

Liu

Lim

et al. 2018

Nat Commun

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“…The expression of A20 has also been investigated in mouse development [20]. Low-level expression was discovered in the CNS of mouse embryos, while high levels of expression of A20 were noticed in human undifferentiated nasopharyngeal carcinoma, head and neck squamous cell carcinoma, breast carcinoma cells, and prostate cancer cells, all indicating that A20 has a role in pathogenesis of various tumor tissue types [21,22]. A recent study observed that A20 was expressed in human glioblastoma cells, and might be a key regulator of NF-κB-mediated O6-alkylating agent resistance [23].…”

Section: Discussionmentioning

confidence: 99%

A20 is overexpressed in glioma cells and may serve as a potential therapeutic target

Guo

Dong

Liu

et al. 2009

Expert Opinion on Therapeutic Targets

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“…A c c e p t e d M a n u s c r i p t 3 Increase of expression: * rat insulin-producing -cells (RINm5F) * human islet cells * liver allografts [107,108] Decrease of expression: * LNCaP cells [106] Zinc depletion Diminished LPS-and TPA-induced expression in promyelocytic leukemia HL-60 cells [84,85] A c c e p t e d M a n u s c r i p t A c c e p t e d M a n u s c r i p t …”

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confidence: 99%

Expression, biological activities and mechanisms of action of A20 (TNFAIP3)

Verstrepen

Verhelst

Loo

et al. 2010

Biochemical Pharmacology

185

160

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A20 (also known as TNFAIP3) is a cytoplasmic protein that plays a key role in the negative regulation of inflammation and immunity. Polymorphisms in the A20 gene locus have been identified as risk alleles for multiple human autoimmune diseases, and A20 has also been proposed to function as a tumor suppressor in several human B-cell lymphomas. A20 expression is strongly induced by multiple stimuli, including the proinflammatory cytokines TNF and IL-1, and microbial products that trigger pathogen recognition receptors, such as Toll-like receptors. A20 functions in a negative feedback loop, which mediates its inhibitory functions by downregulating key proinflammatory signaling pathways, including those controlling NF-κB-and IRF3-dependent gene expression. Activation of these transcription factors is controlled by both K48-and K63-polyubiquitination of upstream signaling proteins, respectively triggering proteasome-mediated degradation or interaction with other signaling proteins. A20 turns off NF-B and IRF3 activation by modulating both types of ubiquitination. Induction of K48-polyubiquitination by A20 involves its C-terminal zincfinger ubiquitin-binding domain, which may promote interaction with E3 ligases, such as Itch and RNF11 that are involved in mediating A20 inhibitory functions. A20 is thought to promote de-ubiquitination of K63-polyubiquitin chains either directly, due to its N-terminal deubiquitinase domain, or by disrupting the interaction between E3 and E2 enzymes that catalyze K63-polyubiquitination. A20 is subject to different mechanisms of regulation, including phosphorylation, proteolytic processing, and association with ubiquitin binding proteins. Here we review the expression and biological activities of A20, as well as the underlying molecular mechanisms.

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A20 gene expression is regulated by TNF, Vitamin D and androgen in prostate cancer cells

Cited by 13 publications

References 30 publications

Enhanced mRNA FISH with compact quantum dots

Enhanced mRNA FISH with compact quantum dots

A20 is overexpressed in glioma cells and may serve as a potential therapeutic target

Expression, biological activities and mechanisms of action of A20 (TNFAIP3)

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