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• W2077492307 abstract "Abstract BACKGROUND: Survival rates for gastrointestinal (GI) and bronchopulmonary (BP) neuroendocrine tumors (NETs) have not altered significantly (5‐year survival rate: GI NETs, 64.1%; BP NETs, 87%‐89%) in 30 years (from 1973 to 2004). No effective or specific antineoplastic agents are available to date, although somatostatin analogs inhibit NET 5‐hydroxytryptophan (5‐HT) secretion. Given the expression of 5‐HT receptors on NETs, the authors hypothesized that 5‐HT autoregulated NET proliferation. METHODS: Proliferation was evaluated in 3 NET cell lines using 3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide uptake; in addition, real‐time polymerase chain reaction analyses and enzyme‐linked immunosorbent assay studies were performed to delineate 5‐HT–mediated signaling pathways. To determine the receptor and role of endogenous 5‐HT production, the effects of ketanserin (5‐HT receptor subtypes 2A and 2C [5‐HT 2A/2C ]); ondansetron (5‐HT 3 ); and the suicide inhibitor of the rate‐limiting enzyme for 5‐HT synthesis, tryptophan hydroxylase (7‐HTP) were investigated. RESULTS: Exogenously added 5‐HT stimulated proliferation in atypical BP NET NCI‐H720 cells (+50%; half‐maximal stimulatory concentration [EC 50 ] = 10 nM), in typical BP NET NCI‐H727 cells (+40%; EC 50 = 0.01 nM), and in GI NET KRJ‐I cells (+60%; EC 50 = 25 nM). In NCI‐H720 cells, proliferation was inhibited by ketanserin (half‐maximal inhibitory concentration [IC 50 ] = 0.06 nM) and ondansetron (IC 50 = 0.4 nM) and also was inhibited by 7‐HTP (IC 50 = 0.3 nM). In NCI‐H727 cells, ketanserin and 7‐HTP inhibited proliferation (IC 50 = 0.3 nM and IC 50 = 2.3 nM, respectively), whereas ondansetron had no effect. In KRJ‐I cells, ketanserin (IC 50 = 0.1 nM) and 7‐HTP (IC 50 = 0.6 nM), but not ondansetron, inhibited proliferation. In all cell lines, 5‐HT activated proliferation through extracellular signal‐regulated kinase 1 (ERK1) and ERK2 phosphorylation and c‐Jun N‐terminal kinase (JNK)‐mediated pathways ( c‐JUN and Ki ‐ 67 transcription). An autoregulatory effect was indicated by the 7‐HTP–mediated inhibition of extracellular 5‐HT and downstream effects on NET proliferation. CONCLUSIONS: Lung and GI NET proliferation was autoregulated by 5‐HT through alterations in ERK and JNK signaling. Targeting NET cells with 5‐HT 2 receptor antagonists and 7‐HTP reversed proliferation. The current results indicated that 5‐HT 2 receptor subtype‐specific antagonists may represent a viable antiproliferative therapeutic strategy. Cancer 2009. © 2009 American Cancer Society." @default.
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• W2077492307 date "2009-07-24" @default.
• W2077492307 modified "2023-10-18" @default.
• W2077492307 title "Autoregulatory effects of serotonin on proliferation and signaling pathways in lung and small intestine neuroendocrine tumor cell lines" @default.
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• W2077492307 doi "https://doi.org/10.1002/cncr.24533" @default.
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