Applying HDACis to increase SSTR2 expression and radiolabeled DOTA-TATE uptake: from cells to mice.

Aims: The aim of our study was to determine the effect of histone deacetylase (HDAC) inhibitors (HDACis) on somatostatin type-2 receptor (SSTR2) expression and [In]In-/[Lu]Lu-DOTA-TATE uptake in vitro and in vivo.

Materials And Methods: The human cell lines NCI-H69 (small-cell lung carcinoma) and BON-1 (pancreatic neuroendocrine tumor) were treated with HDACis (i.e.

Epigenetic regulation of SST expression in small intestinal neuroendocrine tumors.

Background: Somatostatin receptor type 2 (SST) expression is critical for the diagnosis and treatment of neuroendocrine tumors and is associated with improved patient survival. Recent data suggest that epigenetic changes such as DNA methylation and histone modifications play an important role in regulating SST expression and tumorigenesis of NETs. However, there are limited data on the association between epigenetic marks and SST expression in small intestinal neuroendocrine tumors (SI-NETs).

The Effect of VPA Treatment on Radiolabeled DOTATATE Uptake: Differences Observed In Vitro and In Vivo.

To improve peptide receptor radionuclide therapy (PRRT), we aimed to enhance the expression of somatostatin type-2 receptors (SSTR2) in vitro and in vivo, using valproic acid (VPA). Human NCI-H69 small-cell lung carcinoma cells were treated with VPA, followed by [In]In-DOTATATE uptake studies, RT-qPCR and immunohistochemistry analysis. Furthermore, NCI-H69 xenografted mice were treated with VPA or vehicle, followed by [Lu]Lu-DOTATATE injection.

Comparing the Effect of Multiple Histone Deacetylase Inhibitors on SSTR2 Expression and [In]In-DOTATATE Uptake in NET Cells.

The aim of this study was to increase somatostatin type-2 receptor (SSTR2) expression on neuroendocrine tumor (NET) cells using histone deacetylase inhibitors (HDACis), potentially increasing the uptake of SSTR2-targeted radiopharmaceuticals and subsequently improving treatment efficacy of peptide receptor radionuclide therapy (PRRT). Human NET cell lines BON-1, NCI-H727, and GOT1 were treated with HDACis (i.e.