Gene interactions and pathways from curated databases and text-mining

◀ Back to TP53

THBS1 — TP53

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: THBS1 → TP53 (increases, THBS1 Activity)
    Evidence: It is important to note that more than 50% of human cancers contain mutations in p53, and that these mutations can affect the angiogenic balance. Kerbel and colleagues recently reported that cancer cells with p53 mutations are selected for their ability to survive under hypoxic conditions65. As well as their increased resistance to apoptosis, cells with p53 defects have been shown to downregulate the expression of TSP1 and upregulate the expression of VEGFA74.
  • KEGG p53 signaling pathway: TP53 → THBS1 (gene expression, expression)

Text-mined interactions from Literome

Sun et al., Mol Carcinog 1999 (Neoplasm Metastasis) : p53 transcriptionally activates expression of the genes encoding epidermal growth factor receptor, matrix metalloproteinase (MMP)-2, cathepsin D, and thrombospondin-1 but represses expression of the genes encoding basic fibroblast growth factor and multidrug resistance-1
Linderholm et al., Int J Cancer 2000 (Breast Neoplasms...) : Alteration of the p53 gene causes down-regulation of the expression of thrombospondin-1 , a natural inhibitor of angiogenesis
Riewald et al., J Biol Chem 2005 : APC down-regulated transcripts for proapoptotic proteins including p53 and thrombospondin-1, but p53 was unchanged, and thrombospondin was even up-regulated by thrombin
Iwazu et al., Hypertension 2008 (Fibrosis...) : We conclude that exposure to DOCA initially caused the reduced PTC density associated with enhanced apoptosis independent of thrombospondin-1, which induced tubulointerstitial fibrosis via p53 mediated thrombospondin-1 activation, and spironolactone conversely corrected the effects of DOCA to prevent fibrosis
Barillari et al., Atherosclerosis 2010 (Atherosclerosis) : This is followed by an increase in the expression of the p53 induced thrombospondin (TSP)-1 , a VSMC growth and motility factor, and human double minute 2 (HDM2), an antagonist of p53 transcriptional and growth suppressive activity
Sundaram et al., Cancer Res 2011 (Colonic Neoplasms...) : p53-responsive miR-194 inhibits thrombospondin-1 and promotes angiogenesis in colon cancers ... Here, we determined that in HCT116 CRC cells, p53 activates the THBS1 primary transcript, but fails to boost THBS1 mRNA or protein levels, implying posttranscriptional regulation by microRNAs ( miRNA )