Tristetraprolin suppresses AHRR expression through mRNA destabilization

Lee, Hyun Hee; Kim, Won‐Tae; Kim, Dong Hee; Park, Jeong Woo; Kang, Tae-Hong; Chung, Jin Woong; Leem, Sun‐Hee

doi:10.1016/j.febslet.2013.03.031

Cited by 13 publications

(10 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A number of studies have shown that certain metastasis-associated genes with AREs are overexpressed in cancers [34][35][36]. These results are consistent with previous reports that the ARE sequence is important for regulating mRNA stability [32,37]. In the present study, we showed that CRT knockdown suppressed FUT1 mRNA degradation in J82 cells.…”

Section: Discussionsupporting

confidence: 93%

Calreticulin activates β1 integrin via fucosylation by fucosyltransferase 1 in J82 human bladder cancer cells

Chen

Chu

et al. 2014

Biochemical Journal

View full text Add to dashboard Cite

Fucosylation regulates various pathological events in cells. We reported that different levels of CRT (calreticulin) affect the cell adhesion and metastasis of bladder cancer. However, the precise mechanism of tumour metastasis regulated by CRT remains unclear. Using a DNA array, we identified FUT1 (fucosyltransferase 1) as a gene regulated by CRT expression levels. CRT regulated cell adhesion through α1,2-linked fucosylation of β1 integrin and this modification was catalysed by FUT1. To clarify the roles for FUT1 in bladder cancer, we transfected the human FUT1 gene into CRT-RNAi stable cell lines. FUT1 overexpression in CRT-RNAi cells resulted in increased levels of β1 integrin fucosylation and rescued cell adhesion to type-I collagen. Treatment with UEA-1 (Ulex europaeus agglutinin-1), a lectin that recognizes FUT1-modified glycosylation structures, did not affect cell adhesion. In contrast, a FUT1-specific fucosidase diminished the activation of β1 integrin. These results indicated that α1,2-fucosylation of β1 integrin was not involved in integrin-collagen interaction, but promoted β1 integrin activation. Moreover, we demonstrated that CRT regulated FUT1 mRNA degradation at the 3'-UTR. In conclusion, the results of the present study suggest that CRT stabilized FUT1 mRNA, thereby leading to an increase in fucosylation of β1 integrin. Furthermore, increased fucosylation levels activate β1 integrin, rather than directly modifying the integrin-binding sites.

show abstract

Section: Discussionsupporting

confidence: 93%

Calreticulin activates β1 integrin via fucosylation by fucosyltransferase 1 in J82 human bladder cancer cells

Chen

Chu

et al. 2014

Biochemical Journal

View full text Add to dashboard Cite

show abstract

“…TTP is an ARE-binding protein that promotes degradation of ARE-containing mRNAs [2,[8][9][10][11][12][13][14]. Brennan et al [1] reported that TTP expression is significantly decreased in many cancers, and it is possible to suppose that the reason for the increased level of E2F1 in tumor cells, which exert various effects on cell growth and tumor development, may result from the low expression of TTP.…”

Section: Discussionmentioning

confidence: 99%

Tristetraprolin Regulates Prostate Cancer Cell Growth Through Suppression of E2F1

Lee¹,

Lee²,

Leem³

2014

Journal of Microbiology and Biotechnology

Self Cite

View full text Add to dashboard Cite

The transcription factor E2F1 is active during G1 to S transition and is involved in the cell cycle and progression. A recent study reported that increased E2F1 is associated with DNA damage and tumor development in several tissues using transgenic models. Here, we show that E2F1 expression is regulated by tristetraprolin (TTP) in prostate cancer. Overexpression of TTP decreased the stability of E2F1 mRNA and the expression level of E2F1. In contrast, inhibition of TTP using siRNA increased the E2F1 expression. E2F1 mRNA contains three AREs within the 3'UTR, and TTP destabilized a luciferase mRNA that contained the E2F1 mRNA 3'UTR. Analyses of point mutants of the E2F1 mRNA 3'UTR demonstrated that ARE2 was mostly responsible for the TTP-mediated destabilization of E2F1 mRNA. RNA EMSA revealed that TTP binds directly to the E2F1 mRNA 3'UTR of ARE2. Moreover, treatment with siRNA against TTP increased the proliferation of PC3 human prostate cancer cells. Taken together, these results demonstrate that E2F1 mRNA is a physiological target of TTP and suggests that TTP controls proliferation as well as migration and invasion through the regulation of E2F1 mRNA stability.

show abstract

“…miR-mediated gene expression regulation is a well recognized post-transcriptional mechanism that either represses translation and/or destabilizes mRNA transcripts to control protein production (44, 56 -58). Nearly 60% of protein-coding genes are predicted to be targeted by microRNAs and most microRNAs act by base pairing with the 3Ј UTR of the targeted mRNA (59). One gene could potentially be targeted by multiple microRNAs; however, it is unlikely that all of them would be functional at the same time because miRs are expressed in a tissue-and development-specific manner (44, 56 -58, 60).…”

Section: Discussionmentioning

confidence: 99%

Methylxanthines Increase Expression of the Splicing Factor SRSF2 by Regulating Multiple Post-transcriptional Mechanisms

Shi

Pabon

Scotto

2015

Journal of Biological Chemistry

View full text Add to dashboard Cite

Background: Caffeine regulates alternative splicing by increasing SRSF2, normally constrained by a negative feedback loop. Results: Caffeine blocks nonsense-mediated decay, induces 3Ј UTR alternative splicing, and down-regulates SRSF2-targeting microRNAs, thereby breaking the negative feedback loop to increase SRSF2. Conclusion: Caffeine modulates multiple post-transcriptional processes to increase SRSF2. Significance: This study expands our understanding of SRSF2 regulation, and may provide insight into SRSF2 dysregulation in disease.

show abstract

Tristetraprolin suppresses AHRR expression through mRNA destabilization

Abstract: Edited by Ivan Sadowski

Cited by 13 publications

References 32 publications

Calreticulin activates β1 integrin via fucosylation by fucosyltransferase 1 in J82 human bladder cancer cells

Calreticulin activates β1 integrin via fucosylation by fucosyltransferase 1 in J82 human bladder cancer cells

Tristetraprolin Regulates Prostate Cancer Cell Growth Through Suppression of E2F1

Methylxanthines Increase Expression of the Splicing Factor SRSF2 by Regulating Multiple Post-transcriptional Mechanisms

Contact Info

Product

Resources

About