Skip to main content
. 2022 Dec 14;13:1082871. doi: 10.3389/fendo.2022.1082871

Figure 2.

Figure 2

Supposed mechanisms underlying the dual opposing effects of Cystatin C (Cyst C) on urogenital malignancy progression. (A) Tumor-suppressing mechanisms 1) Cathepsin inhibition-dependent: Cyst C may thwart urogenital malignancy progression by inhibiting extracellular cysteine cathepsin activity and, consequently, their contribution to tumor cell migration, invasion, angiogenesis, and metastasis. 2) TGF-β interaction: Cyst C inhibited TGF-β binding to its type II cell surface receptor as well as TGF-β stimulation of initiating metastatic events such as epithelial-to-mesenchymal transition (EMT). 3)Cyst C may also mediate tumor cell invasion by regulating the MAPK/ERK cascade. (B) Cyst C may promote the malignant progression of urogenital malignancy by 1) inhibiting Lysosomal Cathepsins-mediated apoptosis. 2)Regulation of p38 MAPK signaling. 3)Modulation of 14-3-3 (ζ.B) adaptor proteins expression. 4) Damage to the endothelial glycocalyx and increased exposure of shielded adhesion molecules. 5) Impaired antitumor immune response mediated by T cells. 6) Increased expression of tumor-promoting proteinases (for example, cathelipsin B, K, L, S, and legumain).