RT Journal Article
SR Electronic
T1 Interference with ATF5 Function Enhances the Sensitivity of Human Pancreatic Cancer Cells to Paclitaxel-induced Apoptosis
JF Anticancer Research
JO Anticancer Res
FD International Institute of Anticancer Research
SP 4385
OP 4394
VO 32
IS 10
A1 MING HU
A1 BIN WANG
A1 DONGMENG QIAN
A1 LING LI
A1 LI ZHANG
A1 XUXIA SONG
A1 DAVID X. LIU
YR 2012
UL http://ar.iiarjournals.org/content/32/10/4385.abstract
AB Background: Past work has established that human glioblastomas and breast cancer cells invariably express the activating transcription factor 5 (ATF5) and that loss of function of ATF5 caused massive apoptotic death of all cancer cell lines tested. ATF5 expression and function in pancreatic cancer cells have not been investigated. Materials and Methods: Quantitative real-time/reverse transcription-polymerase chain reaction (QRT/RT-PCR), western blotting (WB), immunohistochemistry (IHC) and promoter reporter assay were used for gene expression analysis. MTT [3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay and FACS (fluorescence-activated cell sorting) analysis were used to monitor cell viability/apoptosis. Results: ATF5 is highly expressed in pancreatic cancer cells as compared with non-tumor tissues. Both paclitaxel treatment and loss of function of ATF5 elicited apoptosis of SW1990 cells. Interference with ATF5 function in SW1990 cells resulted in down-regulation of BCL-2 and up-regulation of BAX, resulting in enhanced sensitivity to apoptosis induced by paclitaxel treatment. Conclusion: ATF5 is highly expressed in pancreatic cancer cells. Targeting ATF5 significantly enhances paclitaxel-induced apoptosis in human pancreatic cancer cells. ATF5 could be an important therapeutic target for pancreatic cancer treatment.