Trichostatin A potentiates TRAIL-induced antitumor effects via inhibition of ERK/FOXM1 pathway in gastric cancer View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2016-08

AUTHORS

Lin Li, Biao Fan, Lian-Hai Zhang, Xiao-Fang Xing, Xiao-Jing Cheng, Xiao-Hong Wang, Ting Guo, Hong Du, Xian-Zi Wen, Jia-Fu Ji

ABSTRACT

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is an ideal apoptosis inducer and believed to have promise in cancer therapy, yet part of cancer cells exhibit resistance to TRAIL-mediated apoptosis. This necessitates the exploration of agents that resensitizes cancer cells to TRAIL. In our study, we found that Trichostatin A (TSA), an histone deacetylase (HDAC) inhibitor, augmented TRAIL-induced apoptosis in gastric cancer cells in a caspase-dependent manner. Besides, upregulation of DR5 and downregulation of anti-apoptotic proteins including XIAP, Mcl-1, Bcl-2 and Survivin also contributed to this synergism. Noticeably, TSA treatment inhibited Forkhead boxM1 (FOXM1), which expression level showed negative correlation with TRAIL sensitivity. Similarly, silencing of FOXM1 by small interfering RNA (siRNA) resensitized cancer cells to TRAIL and strengthened the TRAIL-augmenting effect of TSA. In addition, we demonstrated the depletion of FOXM1 was a consequence of the inactivation of ERK mediated by TSA. Collectively, it was first shown that TSA potentiated TRAIL sensitivity via ERK/FOXM1 pathway in gastric cancer cells. FOXM1 might serve as a biomarker for predicting sensitivity to TRAIL. More... »

PAGES

10269-10278

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s13277-016-4816-5

DOI

http://dx.doi.org/10.1007/s13277-016-4816-5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1050816236

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26831669


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