Overexpression of the natural tetrapeptide acetyl‐<i>N</i>‐ser‐asp‐lys‐pro derived from thymosin β4 in neoplastic diseases

Liu, Jian‐Miao; Garcia-Alvarez, Maria-Concepcion; Bignon, Jérôme; Kusiński, Michał; Kuzdak, Krzysztof; Riches, Andrew; Wdzieczak‐Bakala, Joanna

doi:10.1111/j.1749-6632.2010.05488.x

Cited by 22 publications

(32 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However the precise role that ACSDKP serves in leukemia has not yet been elucidated. It was identified that ACSDKP expression is upregulated in human leukemia (17) and it was demonstrated that ACSDKP could enhance the proliferation of U87-MG glioblastoma cells via the PI3KCA/Akt signaling pathway (20). Therefore, the current study aimed to determine the role of ACSDKP in AML.…”

Section: Discussionmentioning

confidence: 97%

“…It has been demonstrated that ACSDKP is associated with endothelial cell proliferation (13), the promotion of angiogenesis (14) and the inhibition of myofibroblast differentiation (15). ACSDKP is also considered to be abnormally expressed in some human malignant tumors, including tumors of the thyroid gland (16), breast, colon, head and neck, kidney, lung, skin, ovary and prostate (17,18). It has been demonstrated that ACSDKP expression varies during chemotherapy to treat patients with AML, in certain patients the ACSDKP level increased sharply during treatment, whereas in others it did not change or decreased (19); however, few studies investigating ACSDKP have been conducted since.…”

Section: Introductionmentioning

confidence: 99%

“…It has been demonstrated that ACSDKP expression varies during chemotherapy to treat patients with AML, in certain patients the ACSDKP level increased sharply during treatment, whereas in others it did not change or decreased (19); however, few studies investigating ACSDKP have been conducted since. It has been demonstrated that ADSCKP is upregulated in human leukemia cells and may enhance the proliferation of U87-MG glioblastoma cells via the phosphatidylinositol 4,5-bisphosphate 3-kinase catalytic subunit α (PI3KCA)/protein kinase B (Akt) signaling pathway (17). Furthermore, it was indicated that prolyl oligopeptidase inhibitor (POPi) may inhibit the stimulation of U87-MG glioblastoma cell proliferation by ADSCKP (20).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Prolyl oligopeptidase inhibitor suppresses the upregulation of ACSDKP in patients with acute myeloid leukemia

Cao

Zhao

et al. 2018

Exp Ther Med

View full text Add to dashboard Cite

Abstract. The aim of the current study was to measure the expression of acetyl-N-Ser-Asp-Lys-Pro (ACSDKP) in patients with acute myeloid leukemia (AML) and the effect of prolyl oligopeptidase inhibitor (POPi) on the bone marrow stromal cells of these patients. Serum and bone marrow stromal cell samples were collected from 33 patients with AML admitted to Wuxi Second People's Hospital, Nanjing Medical University between September 2011 and August 2016. ACSDKP levels were measured using a highly specific competitive enzyme immunoassay (EIA). Bone marrow stromal cells were treated with synthetic ACSDKP (10 µM/ml) or different concentrations of POPi S17092 (25, 50 and 100 µg/ml). Cells that received no treatment were used as control. An MTT assay was conducted to measure the proliferation of bone marrow stromal cells. The results demonstrated that serum levels of ACSDKP in patients with AML were significantly higher than those of controls (P<0.05). Following treatment with ACSDKP, cell proliferation was significantly increased compared with untreated cells (P<0.05). However, following treatment with different concentrations of POPi, the expression of ACSDKP was significantly decreased in a dose-dependent manner (P<0.05). Furthermore, the proliferation of bone marrow stromal cells was also decreased in a dose-dependent manner. Therefore, the present study demonstrated that ACSDKP levels were increased in the serum and bone marrow stromal cells of patients with AML and that ACSDKP promoted the proliferation of bone marrow stromal cells of these patients, which was inhibited by POPi. These results may identify a novel target for the treatment of AML.

show abstract

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Prolyl oligopeptidase inhibitor suppresses the upregulation of ACSDKP in patients with acute myeloid leukemia

Cao

Zhao

et al. 2018

Exp Ther Med

View full text Add to dashboard Cite

show abstract

“…Although the details of the endogenous AcSDKP production pathway are not yet clear, the available evidence suggests that thymosin b4 (Tb4) is the most likely candidate precursor of AcSDKP. 130,131 AcSDKP is the N-terminal sequence of Tb4. Prolyl oligopeptidase may be responsible for the formation of AcSDKP, and prolyl oligopeptidase inhibitors may block the formation of AcSDKP from Tb4.…”

Section: Perspective: Anti-fibrosis Therapymentioning

confidence: 99%

Pathophysiology of the aging kidney and therapeutic interventions

2012

View full text Add to dashboard Cite

Kidneys are among the organs affected by the aging process. Aging kidneys are characterized by progressive scarring and measurable declines in renal function. Deficiencies in renal function are associated with mortality in all populations. Therefore, if the kidneys age at an accelerated rate relative to the other organs in a particular individual, then slowing or reversing the kidney aging process may be a therapeutically useful strategy. In this review, we will discuss the physiology and pathogenesis of kidney aging and analyze potential therapeutic strategies for halting the aging process in the kidneys.

show abstract

“…We previously reported that Ac-SDKP decreased cardiac and renal inflammatory cell infiltration in various models of hypertension, as well as in the model of heart failure after myocardial infarction (27,28,33). In addition, Lin et al (14) demonstrated that Ac-SDKP prevented macrophage infiltration in the aorta in rats with angiotensin II (Ang II)-induced hypertension, and it suppressed ICAM-1 mRNA that is often used as a marker of endothelial cell inflammatory response (15). Furthermore, Nakagawa et al (22) showed that Ac-SDKP reduced ICAM-1 protein expression in experimental autoimmune myocarditis (EAM) (22).…”

mentioning

confidence: 99%

Ac-SDKP suppresses TNF-α-induced ICAM-1 expression in endothelial cells via inhibition of IκB kinase and NF-κB activation

Zhu

Yang

Janic

et al. 2016

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Zhu L, Yang X-P, Janic B, Rhaleb N-E, Harding P, Nakagawa P, Peterson EL, Carretero OA. Ac-SDKP suppresses TNF-␣-induced ICAM-1 expression in endothelial cells via inhibition of IB kinase and NF-B activation. Am J Physiol Heart Circ Physiol 310: H1176 -H1183, 2016. First published March 4, 2016 doi:10.1152/ajpheart.00252.2015.-N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a naturally occurring tetrapeptide that prevents inflammation and fibrosis in hypertension and other cardiovascular diseases. We previously showed that, in angiotensin II-induced hypertension, Ac-SDKP decreased the activation of nuclear transcription factor NF-B, whereas, in experimental autoimmune myocarditis and hypertension animal models, it also reduced the expression of endothelial leukocyte adhesion molecule ICAM-1. However, the mechanisms by which Ac-SDKP downregulated ICAM-1 expression are still unclear. TNF-␣ is a proinflammatory cytokine that induces ICAM-1 expression in various cell types via TNF receptor 1 and activation of the classical NF-B pathway. We hypothesized that in endothelial cells Ac-SDKP suppresses TNF-␣-induced ICAM-1 expression by decreasing IKK phosphorylation that as a consequence leads to a decrease of IB phosphorylation and NF-B activation. To test this hypothesis, human coronary artery endothelial cells were treated with Ac-SDKP and then stimulated with TNF-␣. We found that TNF-␣-induced ICAM-1 expression was significantly decreased by Ac-SDKP in a dose-dependent manner. Ac-SDKP also decreased TNF-␣-induced NF-B translocation from cytosol to nucleus, as assessed by electrophoretic mobility shift assay, which correlated with a decrease in IB phosphorylation. In addition, we found that Ac-SDKP decreased TNF-␣-induced IKK phosphorylation and IKK-␤ expression. However, Ac-SDKP had no effect on TNF-␣-induced phosphorylation of p38 MAP kinase or ERK. Thus we conclude that Ac-SDKP inhibition of TNF-␣ activation of canonical, i.e., IKK-␤-dependent, NF-B pathway and subsequent decrease in ICAM-1 expression is achieved via inhibition of IKK-␤.

show abstract

Overexpression of the natural tetrapeptide acetyl‐N‐ser‐asp‐lys‐pro derived from thymosin β4 in neoplastic diseases

Cited by 22 publications

References 34 publications

Prolyl oligopeptidase inhibitor suppresses the upregulation of ACSDKP in patients with acute myeloid leukemia

Prolyl oligopeptidase inhibitor suppresses the upregulation of ACSDKP in patients with acute myeloid leukemia

Pathophysiology of the aging kidney and therapeutic interventions

Ac-SDKP suppresses TNF-α-induced ICAM-1 expression in endothelial cells via inhibition of IκB kinase and NF-κB activation

Contact Info

Product

Resources

About