✦ LIBER ✦

Gefitinib Inhibits the Proliferation of Pancreatic Cancer Cells via Cell Cycle Arrest

✍ Scribed by Xiaohua Zhou; Maqing Zheng; Fang Chen; Yunxia Zhu; Wei Yong; Haiyan Lin; Yujie Sun; Xiao Han

Publisher: Wiley (John Wiley & Sons)
Year: 2009
Tongue: English
Weight: 281 KB
Volume: 292
Category: Article
ISSN: 1932-8486
DOI: 10.1002/ar.20938

No coin nor oath required. For personal study only.

✦ Synopsis

Abstract

High expression of the epidermal growth factor receptor (EGFR) has been implicated in the development of pancreatic cancer. Gefitinib is an orally active and selective EGFR‐TKI (EGFR‐tyrosine kinase inhibitor) that blocks signal transduction pathways responsible for the proliferation and survival of cancer cells, and other host‐dependent processes promoting cancer growth. This study investigated the anticancer effect of gefitinib on human pancreatic cancer cells and the molecular mechanism involved. We first evaluated the effect of gefitinib on cell proliferation with MTT assay and the results demonstrated that gefitinib significantly inhibited the proliferation of pancreatic cancer cells. Flow cytometric analysis showed that gefitinib induced a delay in cell cycle progression and a G0/G1 arrest together with a G2/M block; these were associated with increased expression of p27^Kip1^ cyclin‐dependent kinase inhibitor combined with decreased expression of aurora B. Besides, luciferase reporter assay revealed that transcriptional mechanism was responsible for the down‐regulation of aurora B protein by gefitinib. Overall, the results suggest a mechanistic connection among these events to provide new insights into the mechanism underlying the antiproliferative effect of gefitinib on pancreatic cancer and supplement a theory basis of gefitinib in clinical treatment of pancreatic cancer. Anat Rec, 292:1122–1127, 2009. © 2009 Wiley‐Liss, Inc.

📜 SIMILAR VOLUMES

Different mechanisms for inhibition of c

Different mechanisms for inhibition of cell proliferation via cell cycle proteins in PC12 cells by nerve growth factor and staurosporine

✍ L. Gollapudi; K.E. Neet 📂 Article 📅 1997 🏛 John Wiley and Sons 🌐 English ⚖ 348 KB 👁 2 views

PC12 cells have previously been shown to cease cell division during nerve growth-factor (NGF)-induced differentiation by affecting specific cell cycle proteins. Staurosporine, a protein kinase inhibitor, also causes PC12 cell differentiation, independently of neurotrophins or plasma membrane recepto

Induction of cell-cycle arrest and apopt

Induction of cell-cycle arrest and apoptosis by a novel retinobenzoic-acid derivative, TAC-101, in human pancreatic-cancer cells

✍ Koji Fujimoto; Ryo Hosotani; Ryuichiro Doi; Michihiko Wada; Jeon-Uk Lee; Takatom 📂 Article 📅 1999 🏛 John Wiley and Sons 🌐 French ⚖ 142 KB 👁 2 views

In this study, we investigated the effect of a novel retinobenzoic acid, 4-[3,5-bis (trimethylsilyl) benzamido] benzoic acid (TAC-101), on the growth of 4 human pancreatic-cancer cell lines; BxPC-3, MIAPaCa-2, CFPAC-1 and AsPC-1. TAC-101 significantly inhibited the proliferation of BxPC-3 and MIA-Pa

Oxytocin inhibits the proliferation of M

Oxytocin inhibits the proliferation of MDA-MB231 human breast-cancer cells via cyclic adenosine monophosphate and protein kinase A

✍ Paola Cassoni; Anna Sapino; Nicoletta Fortunati; Luca Munaron; Bice Chini; Giann 📂 Article 📅 1997 🏛 John Wiley and Sons 🌐 French ⚖ 81 KB

Oxytocin (OT) inhibits the proliferation of breast-cancer cells in vitro via a specific G-coupled receptor. To elucidate the intracellular mechanism involved in this biological effect, different G-coupled receptor mediators have been investigated in untreated and OT-treated MDA-MB231 breastcarcinoma

Opioid agonists modify breast cancer cel

Opioid agonists modify breast cancer cell proliferation by blocking cells to the G2/M phase of the cycle: Involvement of cytoskeletal elements

✍ Simone Panagiotou; Efstathia Bakogeorgou; Evangelia Papakonstanti; Anastassia Ha 📂 Article 📅 1999 🏛 John Wiley and Sons 🌐 English ⚖ 110 KB 👁 1 views

Opioids decrease cell proliferation in different systems including breast, prostate, lung, kidney, and intestine, through an interaction with opioid as well as other membrane-receptor systems (somatostatin, cholinergic), through an unidentified mechanism. Recently, we have reported an interaction of

Amphiregulin antisense oligonucleotide i

Amphiregulin antisense oligonucleotide inhibits the growth of T3M4 human pancreatic cancer cells and sensitizes the cells to EGF receptor-targeted therapy

✍ Hitoshi Funatomi; Jun Itakura; Toshiyuki Ishiwata; Ira Pastan; Stewart A. Thomps 📂 Article 📅 1997 🏛 John Wiley and Sons 🌐 French ⚖ 152 KB 👁 2 views

Human pancreatic cancers overexpress the epidermal growth factor (EGF) receptor (EGFR) and all 5 ligands that bind to this receptor, including amphiregulin. It is not known, however, whether amphiregulin contributes in an autocrine manner to enhance pancreatic cancer cell growth. Therefore, we used