Tristetraprolin Down-Regulates IL-23 Expression in Colon Cancer Cells

Lee, Hyun Hee; Song, Yang; Vo, Mai-Tram; Cho, Wha Ja; Lee, Byung Ju; Leem, Sun‐Hee; Lee, Sang‐Hyun; Jeong, Hee; Park, Jeong Woo

doi:10.1007/s10059-013-0268-6

Cited by 30 publications

(26 citation statements)

References 33 publications

(41 reference statements)

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“…of n ϭ 10 -12 analyses (*, p Ͻ 0. opment and is a predictor of cardiovascular events (2, 3). Endothelial dysfunction is a common feature of patients with atherosclerosis (4) and has been linked to RA-driven systemic inflammation (46). The importance of systemic inflammation in atherogenesis is demonstrated by the correlation of increased concentrations of inflammation markers with cardiovascular mortality in RA patients (45,47).…”

Section: Discussionmentioning

confidence: 99%

Endothelial Dysfunction in Tristetraprolin-deficient Mice Is Not Caused by Enhanced Tumor Necrosis Factor-α Expression

Bollmann¹,

Wu²,

Oelze

et al. 2014

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Endothelial Dysfunction in Tristetraprolin-deficient Mice Is Not Caused by Enhanced Tumor Necrosis Factor-α Expression

Bollmann¹,

Wu²,

Oelze

et al. 2014

Journal of Biological Chemistry

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“…As a direct consequence of its role as a suppressor of inflammatory signaling, loss of TTP in mice results in the elevated levels of circulating cytokines and chronic inflammation [4]. Most of the characterized suppressor functions of TTP have been associated with its known target genes, including inflammatory cytokines, such as IL-8, IL-6 and IL-23 [5][6][7]. In glioma, it is evidenced that interleukin-13 (IL-13) is responsible for migration and invasion of glioma cells, which is equipped with ARE in the 3′-UTR, providing the possibility that TTP inhibits cell invasion and metastasis by degrading IL-13 post-transcriptionally [8].…”

mentioning

confidence: 99%

Effects of Tristetraprolin on Doxorubicin (Adriamycin)-induced experimental nephrotic syndrome though inhibiting IL-13 /STAT6 signal pathway

Zhang¹,

Ge²,

Guo³

et al. 2019

Preprint

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Background: To study the effects of Tristetraprolin (TTP) on Doxorubicin (DOX)-induced experimental kidney injury (KI). Methods: DOX was used to induce kidney injury in Balb/c male mice (in vivo) and in human kidney proximal tubular epithelial cell line (HK-2) and normal rat kidney epithelial cell line (NRK-52E) (in vitro). Body weight of the animal groups under investigation were recorded daily throughout the experimental period. Histological changes were observed using Hematoxylin-eosin (HE) staining, and levels of blood urea nitrogen, serum creatinine and serum cystatin C in KI mice, and ROS, MDA, LDH and SOD in cells were detected using the corresponding kits. Meanwhile, intracellular levels of oxidative stress were assessed using 2, 7-dichlorodihydrofluorescein diacetate (DCF-DA) fluorescent staining. TTP and Kim-1 expression levels were measured by immunohistochemistry and western blot. The TNF-α, IL-1β and IL-6 levels were evaluated by ELISA. Expressions of IL-13, STAT6, p-STAT6, Bcl-2, Bax, cleaved-caspase3 were detected via western blot, respectively. CCK-8 was conducted for analyzing cell viability, and cells apoptosis were assessed by DAPI staining and flow cytometry. Results: DOX treatment decreased body weight and aggravated renal injury without changes in water and food intake. DOX significantly reduced TTP expression, stimulated IL-13/STAT6 pathway and elevated the levels of several factors related to renal injury, including inflammatory response, oxidative stress and cell apoptosis, which were significantly restored by the treatment of overexpression TTP in vitro. Conclusion: Overexpression of TTP significantly reduces DOX-induced adverse outcomes so as to prevent renal injury. Inhibition of IL-13/STAT6 pathway may be the functional mechanism under TTP in experimental KI.

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“…Moreover, a lack of TTP is associated with a variety of cancer-related processes (Brennan et al, 2009). In this respect, regulation of TTP expression has been shown to play a role in several cancers such as colon, breast, skin, lung, and brain (Lee et al, 2013;Suswam et al, 2008). However, its role in glioma has not been fully investigated.…”

Section: Discussionmentioning

confidence: 99%

Tristetraprolin Inhibits the Growth of Human Glioma Cells through Downregulation of Urokinase Plasminogen Activator/Urokinase Plasminogen Activator Receptor mRNAs

Ryu

Yoon

Lee

et al. 2015

Molecules and Cells

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Urokinase plasminogen activator (uPA) and urokinase plasminogen activator receptor (uPAR) play a major role in the infiltrative growth of glioblastoma. Downregulatoion of the uPA and uPAR has been reported to inhibit the growth glioblastoma. Here, we demonstrate that tristetraprolin (TTP) inhibits the growth of U87MG human glioma cells through downregulation of uPA and uPAR. Our results show that expression level of TTP is inversely correlated with those of uPA and uPAR in human glioma cells and tissues. TTP binds to the AU-rich elements within the 3' untranslated regions of uPA and uPAR and overexpression of TTP decreased the expression of uPA and uPAR through enhancing the degradation of their mRNAs. In addition, overexpression of TTP inhibited the growth and invasion of U87MG cells. Our findings implicate that TTP can be used as a promising therapeutic target to treat human glioma.

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Tristetraprolin Down-Regulates IL-23 Expression in Colon Cancer Cells

Cited by 30 publications

References 33 publications

Endothelial Dysfunction in Tristetraprolin-deficient Mice Is Not Caused by Enhanced Tumor Necrosis Factor-α Expression

Endothelial Dysfunction in Tristetraprolin-deficient Mice Is Not Caused by Enhanced Tumor Necrosis Factor-α Expression

Effects of Tristetraprolin on Doxorubicin (Adriamycin)-induced experimental nephrotic syndrome though inhibiting IL-13 /STAT6 signal pathway

Tristetraprolin Inhibits the Growth of Human Glioma Cells through Downregulation of Urokinase Plasminogen Activator/Urokinase Plasminogen Activator Receptor mRNAs

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