Mechanistically, SPARC inhibited tumor apoptosis in colorectal cancer via inhibition of Bcl-2, which is anti-apoptotic, as well as by upregulating autophagy [187]; SPARC also induced cell cycle arrest in medulloblastoma cells at the G2/metaphase transition via upregulation of p21 [188] and in prostate cancer by promoting expression of p21 and p27kip1 [181]; and finally, SPARC blocked intra-tumoral angiogenesis in pancreatic ductal carcinoma cells via direct binding to VEGF and platelet-derived growth factor [189]. Here, SPARC is linked to neoplasm.