Τίτλος:
Current evidence for histone deacetylase inhibitors in pancreatic cancer
Γλώσσες Τεκμηρίου:
Αγγλικά
Περίληψη:
Pancreatic cancer is one of the most aggressive human cancers, with more than 200 000 deaths worldwide every year. Despite recent efforts, conventional treatment approaches, such as surgery and classic chemotherapy, have only slightly improved patient outcomes. More effective and well-tolerated therapies are required to reverse the current poor prognosis of this type of neoplasm. Among new agents, histone deacetylase inhibitors (HDACIs) are now being tested. HDACIs have multiple biological effects related to acetylation of histones and many non-histone proteins that are involved in regulation of gene expression, apoptosis, cell cycle progression and angiogenesis. HDACIs induce cell cycle arrest and can activate the extrinsic and intrinsic pathways of apoptosis in different cancer cell lines. In the present review, the main mechanisms by which HDACIs act in pancreatic cancer cells in vitro, as well as their antiproliferative effects in animal models are presented. HDACIs constitute a promising treatment for pancreatic cancer with encouraging anti-tumor effects, at well-tolerated doses. © 2013 Baishideng. All rights reserved.
Συγγραφείς:
Koutsounas, I.
Giaginis, C.
Patsouris, E.
Theocharis, S.
Περιοδικό:
World Journal of Gastroenterology
Εκδότης:
Baishideng Publishing Group Co
Λέξεις-κλειδιά:
4 phenylbutyric acid; bortezomib; butyric acid; cyclin dependent kinase inhibitor 1C; entinostat; erlotinib; fluorouracil; gemcitabine; histone acetyltransferase; histone deacetylase; histone deacetylase inhibitor; maspin; membrane metalloendopeptidase; methylated DNA protein cysteine methyltransferase; mocetinostat; mucin; nvplbh 589; oxaliplatin; panobinostat; peroxisome proliferator activated receptor; protein p21; protein p27; romidepsin; sorafenib; tacedinaline; transforming growth factor beta; trichostatin A; unclassified drug; valproic acid; vorinostat; zebularine, angiogenesis; apoptosis; autophagy; cancer inhibition; cancer prognosis; cell cycle arrest; cell cycle progression; cell proliferation; chromatin assembly and disassembly; down regulation; gene expression; histone acetylation; human; nonhuman; pancreas cancer; phase 2 clinical trial (topic); phase 3 clinical trial (topic); randomized controlled trial (topic); review; signal transduction; tumor xenograft; upregulation
DOI:
10.3748/wjg.v19.i6.813