<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>3</volume><submitter>Chang JY</submitter><pubmed_abstract>Self-aggregation of transforming growth factor β (TGF-β)1-induced antiapoptotic factor (TIAF1) is known in the nondemented human hippocampus, and the aggregating process may lead to generation of amyloid β (Aβ) for causing neurodegeneration. Here, we determined that overexpressed TIAF1 exhibits as aggregates together with Smad4 and Aβ in the cancer stroma and peritumor capsules of solid tumors. Also, TIAF1/Aβ aggregates are shown on the interface between brain neural cells and the metastatic cancer cell mass. TIAF1 is upregulated in developing tumors, but may disappear in established metastatic cancer cells. Growing neuroblastoma cells on the extracellular matrices from other cancer cell types induced production of aggregated TIAF1 and Aβ. In vitro induction of TIAF1 self-association upreg</pubmed_abstract><journal>Cell death &amp; disease</journal><pagination>e302</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC3358014</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>TIAF1 self-aggregation in peritumor capsule formation, spontaneous activation of SMAD-responsive promoter in p53-deficient environment, and cell death.</pubmed_title><pmcid>PMC3358014</pmcid><pubmed_authors>Chang JY</pubmed_authors><pubmed_authors>Lee MH</pubmed_authors><pubmed_authors>Chen YA</pubmed_authors><pubmed_authors>Yang LY</pubmed_authors><pubmed_authors>Sheu HM</pubmed_authors><pubmed_authors>Lin SR</pubmed_authors><pubmed_authors>He H</pubmed_authors><pubmed_authors>Lai FJ</pubmed_authors><pubmed_authors>Chang NS</pubmed_authors><pubmed_authors>Sze CI</pubmed_authors><pubmed_authors>Chen SJ</pubmed_authors><pubmed_authors>Hsieh CC</pubmed_authors><pubmed_authors>Chou PY</pubmed_authors><pubmed_authors>Chiang MF</pubmed_authors><pubmed_authors>Hsieh TH</pubmed_authors></additional><is_claimable>false</is_claimable><name>TIAF1 self-aggregation in peritumor capsule formation, spontaneous activation of SMAD-responsive promoter in p53-deficient environment, and cell death.</name><description>Self-aggregation of transforming growth factor β (TGF-β)1-induced antiapoptotic factor (TIAF1) is known in the nondemented human hippocampus, and the aggregating process may lead to generation of amyloid β (Aβ) for causing neurodegeneration. Here, we determined that overexpressed TIAF1 exhibits as aggregates together with Smad4 and Aβ in the cancer stroma and peritumor capsules of solid tumors. Also, TIAF1/Aβ aggregates are shown on the interface between brain neural cells and the metastatic cancer cell mass. TIAF1 is upregulated in developing tumors, but may disappear in established metastatic cancer cells. Growing neuroblastoma cells on the extracellular matrices from other cancer cell types induced production of aggregated TIAF1 and Aβ. In vitro induction of TIAF1 self-association upreg</description><dates><release>2012-01-01T00:00:00Z</release><publication>2012 Apr</publication><modification>2026-07-16T23:42:05.245Z</modification><creation>2026-07-12T03:12:10.405Z</creation></dates><accession>S-EPMC3358014</accession><cross_references><pubmed>22534828</pubmed><doi>10.1038/cddis.2012.36</doi></cross_references></HashMap>