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• W4281955601 abstract "This study reports that hairy and enhancer of split homolog-1 (HES1), known to repress gene transcription in progenitor cells of several cell lineages, was strongly expressed in cells and tissues of T-cell lymphoma expressing the oncogenic chimeric tyrosine kinase nucleophosmin (NPM)–anaplastic lymphoma kinase [ALK; ALK+ T-cell lymphoma (TCL)]. The structural analysis of the Orange domain of HES1 indicated that HES1 formed a highly stable homodimer. Of note, repression of HES1 expression led to inhibition of ALK+ TCL cell growth in vivo. The expression of the HES1 gene was induced by NPM-ALK through activation of STAT3, which bound to the gene's promoter and induced the gene's transcription. NPM-ALK also directly phosphorylated HES1 protein. In turn, HES1 up-regulated and down-regulated in ALK+ TCL cells, the expression of numerous genes, protein products of which are involved in key cell functions, such as cell proliferation and viability. Among the genes inhibited by HES1 was thioredoxin-interacting protein (TXNIP), encoding a protein implicated in promotion of cell death in various types of cells. Accordingly, ALK+ TCL cells and tissues lacked expression of TXNIP, and its transcription was co-inhibited by HES1 and STAT3 in an NPM-ALK–dependent manner. Finally, the induced expression of TXNIP induced massive apoptotic cell death of ALK+ TCL cells. The results reveal a novel NPM-ALK–controlled pro-oncogenic regulatory network and document an important role of HES and TXNIP in the NPM-ALK–driven oncogenesis, with the former protein displaying oncogenic and the latter tumor suppressor properties. This study reports that hairy and enhancer of split homolog-1 (HES1), known to repress gene transcription in progenitor cells of several cell lineages, was strongly expressed in cells and tissues of T-cell lymphoma expressing the oncogenic chimeric tyrosine kinase nucleophosmin (NPM)–anaplastic lymphoma kinase [ALK; ALK+ T-cell lymphoma (TCL)]. The structural analysis of the Orange domain of HES1 indicated that HES1 formed a highly stable homodimer. Of note, repression of HES1 expression led to inhibition of ALK+ TCL cell growth in vivo. The expression of the HES1 gene was induced by NPM-ALK through activation of STAT3, which bound to the gene's promoter and induced the gene's transcription. NPM-ALK also directly phosphorylated HES1 protein. In turn, HES1 up-regulated and down-regulated in ALK+ TCL cells, the expression of numerous genes, protein products of which are involved in key cell functions, such as cell proliferation and viability. Among the genes inhibited by HES1 was thioredoxin-interacting protein (TXNIP), encoding a protein implicated in promotion of cell death in various types of cells. Accordingly, ALK+ TCL cells and tissues lacked expression of TXNIP, and its transcription was co-inhibited by HES1 and STAT3 in an NPM-ALK–dependent manner. Finally, the induced expression of TXNIP induced massive apoptotic cell death of ALK+ TCL cells. The results reveal a novel NPM-ALK–controlled pro-oncogenic regulatory network and document an important role of HES and TXNIP in the NPM-ALK–driven oncogenesis, with the former protein displaying oncogenic and the latter tumor suppressor properties. This Month in AJPThe American Journal of PathologyVol. 192Issue 8PreviewThe mechanisms underlying alveolar capillary dysplasia (ACD) are unclear. Using patient groups with ACD, pulmonary arterial hypertension (PAH), and healthy controls, Kamp and Neubert et al (Am J Pathol 2022, 1110–1121) studied the microvascular morphology in ACD and the underlying molecular background. Nucleic acid and protein level differences were found in ACD and PAH groups. TEK receptor tyrosine kinase (TIE2)–positive macrophages were markedly increased in ACD, which was characterized by dysfunctional capillaries and a high incidence of intussusceptive angiogenesis. Full-Text PDF" @default.
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• W4281955601 date "2022-08-01" @default.
• W4281955601 modified "2023-10-04" @default.
• W4281955601 title "Induction of Transcriptional Inhibitor HES1 and the Related Repression of Tumor-Suppressor TXNIP Are Important Components of Cell-Transformation Program Imposed by Oncogenic Kinase NPM-ALK" @default.
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• W4281955601 cites W1995762247 @default.
• W4281955601 cites W1998443910 @default.
• W4281955601 cites W2007739717 @default.
• W4281955601 cites W2011937137 @default.
• W4281955601 cites W2023561138 @default.
• W4281955601 cites W2025651276 @default.
• W4281955601 cites W2027337735 @default.
• W4281955601 cites W2034902084 @default.
• W4281955601 cites W2036906474 @default.
• W4281955601 cites W2038586807 @default.
• W4281955601 cites W2042962276 @default.
• W4281955601 cites W2051083170 @default.
• W4281955601 cites W2056946418 @default.
• W4281955601 cites W2058210960 @default.
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• W4281955601 cites W2065522875 @default.
• W4281955601 cites W2068510450 @default.
• W4281955601 cites W2078396922 @default.
• W4281955601 cites W2078658900 @default.
• W4281955601 cites W2088969512 @default.
• W4281955601 cites W2095696852 @default.
• W4281955601 cites W2098272219 @default.
• W4281955601 cites W2112235640 @default.
• W4281955601 cites W2117739778 @default.
• W4281955601 cites W2124478432 @default.
• W4281955601 cites W2131595966 @default.
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• W4281955601 doi "https://doi.org/10.1016/j.ajpath.2022.05.005" @default.
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