BACKGROUND: Thymosin beta 4 (T beta 4) has been shown to be associated with tumor metastasis and angiogenesis; however, its role in pancreatic cancer has not been understood. In the current study, we examined the expression of T beta 4 in pancreatic cancer cells, and determined the effect of exogenous T beta 4 on cytokine secretion, and signal transduction in human pancreatic cancer cells. RESULTS: Pancreatic cancer cell lines expressed higher amount of T beta 4 mRNA than normal human pancreatic ductal epithelium (HPDE) cells. Exogenous T beta 4 increased the secretion of proinflammatory cytokines IL-6, IL-8 and MCP-1 in Panc-1 cells. In addition, T beta 4 activated Jun N-terminal Kinase (JNK) signaling pathways in pancreatic cancer cells. METHODS: The mRNA levels of T beta 4 were determined by real-time RT PCR. Phosphorylation of JNK in pancreatic cancer cells was determined using Bio-Plex phosphoprotein assay. The expression of cytokines in human pancreatic cancer cell lines was determined with Bio-Plex cytokine assay. CONCLUSIONS: T beta 4 might be involved in stimulating human pancreatic cancer progression by promoting proinflammatory cytokine environment and activating JNK signaling pathway. Targeting T beta 4 and related molecules may be a novel therapeutic strategy for pancreatic cancer.
BACKGROUND:Thymosin beta 4 (T beta 4) has been shown to be associated with tumor metastasis and angiogenesis; however, its role in pancreatic cancer has not been understood. In the current study, we examined the expression of T beta 4 in pancreatic cancer cells, and determined the effect of exogenous T beta 4 on cytokine secretion, and signal transduction in humanpancreatic cancer cells. RESULTS:Pancreatic cancer cell lines expressed higher amount of T beta 4 mRNA than normal humanpancreatic ductal epithelium (HPDE) cells. Exogenous T beta 4 increased the secretion of proinflammatory cytokines IL-6, IL-8 and MCP-1 in Panc-1 cells. In addition, T beta 4 activated Jun N-terminal Kinase (JNK) signaling pathways in pancreatic cancer cells. METHODS: The mRNA levels of T beta 4 were determined by real-time RT PCR. Phosphorylation of JNK in pancreatic cancer cells was determined using Bio-Plex phosphoprotein assay. The expression of cytokines in humanpancreatic cancer cell lines was determined with Bio-Plex cytokine assay. CONCLUSIONS:T beta 4 might be involved in stimulating humanpancreatic cancer progression by promoting proinflammatory cytokine environment and activating JNK signaling pathway. Targeting T beta 4 and related molecules may be a novel therapeutic strategy for pancreatic cancer.
Authors: Louis W Feurino; Yuqing Zhang; Uddalak Bharadwaj; Rongxin Zhang; Fei Li; William E Fisher; F Charles Brunicardi; Changyi Chen; Qizhi Yao; L Min Journal: Cancer Biol Ther Date: 2007-07 Impact factor: 4.742
Authors: Buckminster Farrow; Yuko Sugiyama; Andy Chen; Ekong Uffort; William Nealon; B Mark Evers Journal: Ann Surg Date: 2004-06 Impact factor: 12.969
Authors: Christopher F Spurney; Hee-Jae Cha; Arpana Sali; Gouri S Pandey; Emidio Pistilli; Alfredo D Guerron; Heather Gordish-Dressman; Eric P Hoffman; Kanneboyina Nagaraju Journal: PLoS One Date: 2010-01-29 Impact factor: 3.240
Authors: Ming Li; Laszlo Radvanyi; Bingnan Yin; Kiera Rycaj; Jia Li; Raghavender Chivukula; Kevin Lin; Yue Lu; JianJun Shen; David Z Chang; Donghui Li; Gary L Johanning; Feng Wang-Johanning Journal: Clin Cancer Res Date: 2017-07-05 Impact factor: 12.531
Authors: Barbara M Grüner; Hannes Hahne; Pawel K Mazur; Marija Trajkovic-Arsic; Stefan Maier; Irene Esposito; Evdokia Kalideris; Christoph W Michalski; Jörg Kleeff; Sandra Rauser; Roland M Schmid; Bernhard Küster; Axel Walch; Jens T Siveke Journal: PLoS One Date: 2012-06-26 Impact factor: 3.240