Knockdown of glucose-regulated protein 78 enhances poly(ADP-ribose) polymerase cleavage in human pancreatic cancer cells exposed to endoplasmic reticulum stress

被引：16

作者：

Jiang, Xia ^{[1
]}

Kanda, Tatsuo ^{[1
]}

Nakamoto, Shingo ^{[1
,2
]}

Haga, Yuki ^{[1
]}

Sasaki, Reina ^{[1
]}

Nakamura, Masato ^{[1
]}

Wu, Shuang ^{[1
]}

Mikata, Rintaro ^{[1
]}

Yokosuka, Osamu ^{[1
]}

机构：

[1] Chiba Univ, Dept Gastroenterol & Nephrol, Grad Sch Med, Chuo Ku, Chiba 2608677, Japan

[2] Chiba Univ, Dept Mol Virol, Grad Sch Med, Chuo Ku, Chiba 2608677, Japan

来源：

ONCOLOGY REPORTS | 2014年 / 32卷 / 06期

关键词：

apoptosis; ER stress; GRP78/Bip; pancreatic cancer; resistance; UPR; ER STRESS; HEPATOCELLULAR-CARCINOMA; ANDROGEN RECEPTOR; BREAST-CANCER; APOPTOSIS; GRP78; HEPATOCARCINOGENESIS; INVOLVEMENT; ACTIVATION; PATHWAY;

D O I：

10.3892/or.2014.3533

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

The present study examined the expression of glucose-regulated protein 78 (GRP78/Bip) in human pancreatic cancer cell lines and the effect of knockdown of GRP78 on the cleavage of poly(ADP-ribose) polymerase (PARP). Human pancreatic cancer cell lines (KP-2, MIAPaCa-2, Panc-1 and SUIT-2), constitutively expressed GRP78. We also demonstrated that ER stress induced by thapsigargin upregulated protein levels of GRP78. In the presence of thapsigargin, knockdown of GRP78 enhanced the PARP cleavage in the human pancreatic cancer cells. These results provide evidence that GRP78 is a potential therapeutic target for 'difficult-to-treat' pancreatic cancer, in which ER stress signaling in part falls into disorder.

引用

页码：2343 / 2348

页数：6

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