2006
DOI: 10.1677/erc.1.01249
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Antiproliferative and proapoptotic effects of histone deacetylase inhibitors on gastrointestinal neuroendocrine tumor cells

Abstract: Treatment options of advanced neuroendocrine tumors (NETs) are unsatisfactory. Hence, innovative therapeutic approaches are urgently needed. Inhibition of histone deacetylases (HDACs) is a promising new approach in cancer therapy. While several HDAC inhibitors have already entered clinical trials, the effect of HDAC inhibition on NET has not been investigated. Therefore, we evaluated the antineoplastic effects of three different HDAC inhibitors, trichostatin A (TSA), sodium butyrate (NaB), and MS-275, on growt… Show more

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Cited by 68 publications
(55 citation statements)
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“…Submicromolar concentrations of MS-275 were already sufficient to significantly inhibit the proliferation of EGI-1 and TFK-1 cells, and the concentration needed to induce halfmaximal anti-neoplastic effects (IC 50 value) was approximately 0.5 µmol/L in both cell lines. This is comparable to our previous findings on the effects of MS-275 on the growth of gastrointestinal neuroendocrine tumor cells [24] . Recent studies have shown that inhibition of HDAC activity induces apoptosis in a variety of cancers, including breast and prostate cancer, neuroblastoma, hepatoma, gastrointestinal neuroendocrine tumor cells and some types of hematologic malignancies [24,[32][33][34] .…”
Section: Discussionsupporting
confidence: 92%
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“…Submicromolar concentrations of MS-275 were already sufficient to significantly inhibit the proliferation of EGI-1 and TFK-1 cells, and the concentration needed to induce halfmaximal anti-neoplastic effects (IC 50 value) was approximately 0.5 µmol/L in both cell lines. This is comparable to our previous findings on the effects of MS-275 on the growth of gastrointestinal neuroendocrine tumor cells [24] . Recent studies have shown that inhibition of HDAC activity induces apoptosis in a variety of cancers, including breast and prostate cancer, neuroblastoma, hepatoma, gastrointestinal neuroendocrine tumor cells and some types of hematologic malignancies [24,[32][33][34] .…”
Section: Discussionsupporting
confidence: 92%
“…This is comparable to our previous findings on the effects of MS-275 on the growth of gastrointestinal neuroendocrine tumor cells [24] . Recent studies have shown that inhibition of HDAC activity induces apoptosis in a variety of cancers, including breast and prostate cancer, neuroblastoma, hepatoma, gastrointestinal neuroendocrine tumor cells and some types of hematologic malignancies [24,[32][33][34] . The mechanisms involved in the HDAC inhibitorinduced apoptosis are complex and differ among cell types [35] .…”
Section: Discussionsupporting
confidence: 92%
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“…DNA methylases inhibitor and HDAC inhibitor have been extensively used in vitro in both PanNET and small intestine cell lines showing results in terms of reducing cell viability and increasing gene expression (Baradari et al 2006, Habbe et al 2007, Alexander et al 2010, Arvidsson et al 2016. Interestingly, Decitabine increased the expression of SSTR2 and the Ga-DOTATOC uptake in BON1 tumour-bearing mice, indicating a possible therapy implication in re-expression the target for somatostatin receptor-based radiotherapy (Taelman et al 2016).…”
Section: Clinical Implicationmentioning
confidence: 99%
“…The up-regulation of p21 is essential for DNA damage-induced G1 or G2/M phases of the cell cycle arrest in human leukaemia, endometrial or ovarian cancer cell lines Petrella et al, 2008). Additionally, a recent study has shown that p27 is a major inhibitor of cyclin B1 and CDK1, and it can induce G2/M arrest (Baradari et al, 2006). Interestingly, Ueda et al (2007) reported that apicidin markedly up-regulated the expression of p21 and p27, but not p16 and cyclin B expression.…”
Section: Discussionmentioning
confidence: 99%