FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2344122381> ?p ?o ?g. }

• W2344122381 endingPage "5769" @default.
• W2344122381 startingPage "5759" @default.
• W2344122381 abstract "The ability of breast cancer cells to resist anoikis, apoptosis caused by detachment of the non-malignant epithelial cells from the extracellular matrix (ECM), is thought to be critical for breast tumor growth, invasion and metastasis. ErbB2, an oncoprotein that is often overproduced in breast tumors, can block breast cancer cell anoikis via mechanisms that are understood only in part. In an effort to understand them better we found that detachment of the non-malignant human breast epithelial cells from the ECM upregulates a protein Perp in these cells. Perp is a component of the desmosomes, multiprotein complexes involved in cell-to-cell adhesion. Perp can cause apoptosis via unknown mechanisms. We demonstrated that Perp upregulation by cell detachment is driven by detachment-induced loss of epidermal growth factor receptor (EGFR). We also found that Perp knockdown by RNA interference (RNAi) rescues detached cells from death which indicates that Perp contributes to their anoikis. We observed that ErbB2, when overexpressed in detached breast epithelial cells, causes Perp downregulation. Furthermore, ErbB2-directed RNAi or treatment with lapatinib, an ErbB2/EGFR small-molecule inhibitor used for breast cancer therapy, upregulated Perp in ErbB2-positive human breast and ovarian carcinoma cells. We established that ErbB2 downregulates Perp by activating an ErbB2 effector protein kinase Mek that blocks detachment-induced EGFR loss in a manner that requires the presence of a signaling protein Sprouty-2. Finally, we observed that restoration of the wild-type Perp levels in ErbB2-overproducing breast epithelial cells increases their anoikis susceptibility and blocks their clonogenicity in the absence of adhesion to the ECM. In summary, we have identified a novel mechanism of ErbB2-mediated mechanism of anoikis resistance of ErbB2-overproducing breast epithelial cells. This mechanism allows such cells to grow without adhesion to the ECM and is driven by ErbB2-induced activation of Mek, subsequent EGFR upregulation and further EGFR-dependent Perp loss." @default.
• W2344122381 created "2016-06-24" @default.
• W2344122381 creator A5019574388 @default.
• W2344122381 creator A5019948202 @default.
• W2344122381 creator A5049168429 @default.
• W2344122381 creator A5053460625 @default.
• W2344122381 creator A5063410253 @default.
• W2344122381 creator A5074266795 @default.
• W2344122381 creator A5076009109 @default.
• W2344122381 creator A5078364744 @default.
• W2344122381 date "2016-04-25" @default.
• W2344122381 modified "2023-09-25" @default.
• W2344122381 title "ErbB2-dependent downregulation of a pro-apoptotic protein Perp is required for oncogenic transformation of breast epithelial cells" @default.
• W2344122381 cites W1529396499 @default.
• W2344122381 cites W1896854564 @default.
• W2344122381 cites W1924119154 @default.
• W2344122381 cites W1964321121 @default.
• W2344122381 cites W1964596167 @default.
• W2344122381 cites W1967647822 @default.
• W2344122381 cites W1975408970 @default.
• W2344122381 cites W1977252673 @default.
• W2344122381 cites W1978344336 @default.
• W2344122381 cites W1981813507 @default.
• W2344122381 cites W1982967858 @default.
• W2344122381 cites W1983821491 @default.
• W2344122381 cites W1990507126 @default.
• W2344122381 cites W1990562295 @default.
• W2344122381 cites W1994683536 @default.
• W2344122381 cites W1997656209 @default.
• W2344122381 cites W1998662212 @default.
• W2344122381 cites W1999895549 @default.
• W2344122381 cites W2003590580 @default.
• W2344122381 cites W2004510380 @default.
• W2344122381 cites W2007572328 @default.
• W2344122381 cites W2022725013 @default.
• W2344122381 cites W2032415249 @default.
• W2344122381 cites W2032461554 @default.
• W2344122381 cites W2035936653 @default.
• W2344122381 cites W2039074795 @default.
• W2344122381 cites W2042905219 @default.
• W2344122381 cites W2044922611 @default.
• W2344122381 cites W2049533157 @default.
• W2344122381 cites W2056881172 @default.
• W2344122381 cites W2059071562 @default.
• W2344122381 cites W2059815857 @default.
• W2344122381 cites W2071946945 @default.
• W2344122381 cites W2072737818 @default.
• W2344122381 cites W2075768064 @default.
• W2344122381 cites W2076242748 @default.
• W2344122381 cites W2080415915 @default.
• W2344122381 cites W2093859970 @default.
• W2344122381 cites W2095156669 @default.
• W2344122381 cites W2095424453 @default.
• W2344122381 cites W2102943306 @default.
• W2344122381 cites W2104670195 @default.
• W2344122381 cites W2109439031 @default.
• W2344122381 cites W2111532181 @default.
• W2344122381 cites W2111578514 @default.
• W2344122381 cites W2114941442 @default.
• W2344122381 cites W2117563256 @default.
• W2344122381 cites W2121627701 @default.
• W2344122381 cites W2123206362 @default.
• W2344122381 cites W2124891058 @default.
• W2344122381 cites W2136028592 @default.
• W2344122381 cites W2137022580 @default.
• W2344122381 cites W2142076829 @default.
• W2344122381 cites W2144884298 @default.
• W2344122381 cites W2148591855 @default.
• W2344122381 cites W2149444460 @default.
• W2344122381 cites W2151322467 @default.
• W2344122381 cites W2152573992 @default.
• W2344122381 cites W2155363874 @default.
• W2344122381 cites W2159732577 @default.
• W2344122381 cites W2160926271 @default.
• W2344122381 cites W2184278156 @default.
• W2344122381 cites W4243385699 @default.
• W2344122381 doi "https://doi.org/10.1038/onc.2016.109" @default.
• W2344122381 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/27109096" @default.
• W2344122381 hasPublicationYear "2016" @default.
• W2344122381 type Work @default.
• W2344122381 sameAs 2344122381 @default.
• W2344122381 citedByCount "19" @default.
• W2344122381 countsByYear W23441223812017 @default.
• W2344122381 countsByYear W23441223812018 @default.
• W2344122381 countsByYear W23441223812019 @default.
• W2344122381 countsByYear W23441223812020 @default.
• W2344122381 countsByYear W23441223812021 @default.
• W2344122381 countsByYear W23441223812022 @default.
• W2344122381 crossrefType "journal-article" @default.
• W2344122381 hasAuthorship W2344122381A5019574388 @default.
• W2344122381 hasAuthorship W2344122381A5019948202 @default.
• W2344122381 hasAuthorship W2344122381A5049168429 @default.
• W2344122381 hasAuthorship W2344122381A5053460625 @default.
• W2344122381 hasAuthorship W2344122381A5063410253 @default.
• W2344122381 hasAuthorship W2344122381A5074266795 @default.
• W2344122381 hasAuthorship W2344122381A5076009109 @default.
• W2344122381 hasAuthorship W2344122381A5078364744 @default.
• W2344122381 hasBestOaLocation W23441223811 @default.

• next