Background: The natural tetrapeptide acetyl-Ser-Asp-Lys-Pro (AcSDKP), generated from thymosin beta4 following its cleavage by prolyl oligopeptidase (POP), is a physiological stimulator of angiogenesis. Because of the critical role of neovascularisation in tumor development, the expression of AcSDKP and the activity of POP were examined in different human solid malignancies.

Materials And Methods: The expression of AcSDKP and the activity of POP were evaluated in human blood samples and tissue specimens of thyroid goiter and thyroid papillary carcinoma as well as in commercial cancer tissue microarray.

Results: A significantly increased concentration of AcSDKP in intratumoral blood and enhanced tissular activity of POP were detected in cancer patients. The expression of AcSDKP in human breast, colon, head and neck, kidney, lung, skin, ovary and prostate cancer tissues was shown to be greater than that in normal tissues.

Conclusion: AcSDKP and POP contribute to the malignant phenotype and these molecules are potentiel markers of cancer.

Download full-text PDF

Source

Publication Analysis

Top Keywords

expression acsdkp
12
activity pop
12
acsdkp human
8
acsdkp activity
8
acsdkp
7
pop
5
overexpression angiogenic
4
angiogenic tetrapeptide
4
tetrapeptide acsdkp
4
human
4

Similar Publications

Identification of FGFR4 as a regulator of myofibroblast differentiation in pulmonary fibrosis.

Am J Physiol Lung Cell Mol Physiol

December 2024

Université Paris Cité, Institut National de la Santé et de la Recherche Médicale, UMR1152, FHU APOLLO, Labex INFLAMEX, Faculté de médecine Xavier Bichat, Paris, France.

Idiopathic pulmonary fibrosis (IPF) is a devastating lung disease with limited therapeutic options. Fibroblast growth factor receptor-4 (FGFR4) is a known receptor for several paracrine fibroblast growth factors (FGFs). FGFR4 is also the main receptor for FGF19, an endocrine FGF that was demonstrated by our group to have antifibrotic properties in the lung.

View Article and Find Full Text PDF

Ac-SDKP attenuates ER stress-stimulated collagen production in cardiac fibroblasts by inhibiting CHOP-mediated NF-κB expression.

Front Pharmacol

March 2024

Department of Internal Medicine, Hypertension and Vascular Research Division, Henry Ford Hospital, Detroit, MI, United States.

Inflammation and cardiac fibrosis are prevalent pathophysiologic conditions associated with hypertension, cardiac remodeling, and heart failure. Endoplasmic reticulum (ER) stress triggers the cells to activate unfolded protein responses (UPRs) and upregulate the ER stress chaperon, enzymes, and downstream transcription factors to restore normal ER function. The mechanisms that link ER stress-induced UPRs upregulation and NF-κB activation that results in cardiac inflammation and collagen production remain elusive.

View Article and Find Full Text PDF

Kinesin family member 3 A (KIF3A) decrease have been reported in silicotic patients and rats. However, the detailed mechanisms of KIF3A in silicosis remain unknown. In this study, we demonstrated that KIF3A effectively blocked the expression of β-catenin and downstream myocardin-related transcription factor (MRTF)-A/serum response factor (SRF) signaling, thus inhibiting silica-induced epithelial-myofibroblast transition (EMyT).

View Article and Find Full Text PDF
Article Synopsis
  • Prolyl endopeptidase (PREP) is linked to various health issues like inflammation and metabolic dysfunctions, particularly in conditions like metabolic dysfunction-associated fatty liver disease (MAFLD).
  • The study used a high-fat diet (HFD) mouse model to observe changes in the PREP system over time and assessed the effects of the PREP inhibitor KYP-2047 on the condition.
  • Results showed that increased PREP activity worsens liver damage and inflammation in MAFLD, while KYP-2047 improved liver health and metabolism, suggesting it could be a potential treatment for the disease.
View Article and Find Full Text PDF

Polycystic ovary syndrome (PCOS) is an endocrine disorder and metabolic syndrome. Ovarian fibrosis pathological change in PCOS has gradually attracted people's attention. In this study, we constructed a PCOS mouse model through the use of dehydroepiandrosterone.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!