ArticleActa histochemica et cytochemica2022
Cathepsin D Inhibits Angiogenesis in Pituitary Neuroendocrine Tumors.
Article in Acta histochemica et cytochemica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 0 citations in OpenAlex.
- Profiles of FGF2, HGF, Fas/CD95, CASP9, ALDH1A1, and GLUT1 in GEP-NETs: A Comparative Tumor-Margin Study Based on Protein Concentration.International journal of molecular sciences · 2026Article
- The metastatic spectrum in functional and non-functional NENs: mechanistic insights from multi-omics.Frontiers in endocrinology · 2026Review
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Authors and funding
7 authors at 4 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Prolactin and growth hormone can acquire anti-angiogenic properties after undergoing proteolytic cleavage by Cathepsin D and bone morphogenetic protein 1 (BMP-1) into fragments known as vasoinhibins. Little is known about the effect of vasoinhibins on angiogenesis through the involvement of key cleavage enzymes Cathepsin D and BMP-1 in pituitary neuroendocrine tumors (PitNETs, formerly pituitary adenomas). The purpose of this study was to investigate the mechanism of action of Cathepsin D and BMP-1 on angiogenesis in PitNETs compared with that of pro-angiogenic factors, including vascular endothelial growth factor (VEGF) and basic fibroblast growth factor-2 (FGF2). A total of 43 patients were enrolled in a retrospective analysis and 22 samples were suitable for RNA extraction, including 16 nonfunctional PitNETs and six somatotroph tumors. The mRNA and protein levels of Cathepsin D, BMP-1, VEGF, and FGF2 were compared with those of von Willebrand factor, which was assessed to determine the vascularization of PitNETs. Cathepsin D and FGF2 were significantly correlated with vascularization in PitNETs. Both Cathepsin D and FGF2 are highly involved in angiogenesis in PitNETs, although the effect of Cathepsin D as an anti-angiogenic factor is dominant over that of FGF2 as a pro-angiogenic factor.
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