Literature DB >> 23225424

Gefitinib and gemcitabine coordinately inhibited the proliferation of cholangiocarcinoma cells.

Yoshimi Nakajima1, Hitoshi Takagi, Satoru Kakizaki, Norio Horiguchi, Ken Sato, Noriaki Sunaga, Masatomo Mori.   

Abstract

BACKGROUND: Cholangiocarcinoma (CCC) is the second most common type of primary liver cancer, and is associated with a high rate of mortality due to the difficulty of early detection and resistance to chemotherapeutic agents. To evaluate the possibility for new therapeutic strategies, we examined the combined effect of gefitinib and gemcitabine on CCC.
MATERIALS AND METHODS: The effect of gefitinib, an inhibitor of epidermal growth factor receptor (EGFR) signaling, gemcitabine, which is a pyrimidine analog, and the combined effect of gefitinib and gemcitabine on CCC cells were evaluated both in vitro and in vivo.
RESULTS: EGFR mRNA expression and phosphorylation of EGFR were elevated in both human CCC cell lines studied, HuCCT1 and RBE, suggesting EGFR signaling is up-regulated in CCC cell lines. Gefitinib treatment at high concentration inhibited the proliferation of the CCC cell lines. Furthermore, gefitinib reduced the transforming growth factor alpha (TGFα)-induced proliferation of these cells. Gemcitabine also suppressed the growth of the CCC cell lines in a concentration-dependent manner. The combination of gefitinib and gemcitabine synergistically suppressed the growth of the CCC cell lines and induced greater apoptosis compared to the use of either agent alone. As a mechanism for this effect, we found less phosphorylation of the extracellular signal-regulated kinase (ERK) protein, which means the suppression of EGFR signaling, when these compounds were administered together. Cell transplantation assay dramatically demonstrated the synergistic effect of this combination on HuCCT1 xenografts in vivo.
CONCLUSION: The combination of gefitinib and gemcitabine inhibited the proliferation of CCC cells via induction of apoptosis. The combination of EGFR inhibitor and additional chemicals could be a new therapeutic approach for CCC.

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Year:  2012        PMID: 23225424

Source DB:  PubMed          Journal:  Anticancer Res        ISSN: 0250-7005            Impact factor:   2.480


  4 in total

1.  The Effect of the EGFR - Targeting Compound 3-[(4-Phenylpyrimidin-2-yl) Amino] Benzene-1-Sulfonamide (13f) against Cholangiocarcinoma Cell Lines.

Authors:  Papavee Samatiwat; Lueacha Tabtimmai; Prapasiri Suphakun; Nattanan Jiwacharoenchai; Borvorrnvat Toviwek; Veerapol Kukongviriyapan; M Paul Gleeson; Kiattawee Choowongkomon
Journal:  Asian Pac J Cancer Prev       Date:  2021-02-01

2.  Establishment of a human 3D lung cancer model based on a biological tissue matrix combined with a Boolean in silico model.

Authors:  Anna T Stratmann; David Fecher; Gaby Wangorsch; Claudia Göttlich; Thorsten Walles; Heike Walles; Thomas Dandekar; Gudrun Dandekar; Sarah L Nietzer
Journal:  Mol Oncol       Date:  2013-12-18       Impact factor: 6.603

3.  In Vitro and In Vivo Inhibitory Effects of α-Mangostin on Cholangiocarcinoma Cells and Allografts

Authors:  Ratchadawan Aukkanimart; Thidarut Boonmars; Pranee Sriraj; Panupan Sripan; Jiraporn Songsri; Panaratana Ratanasuwan; Porntip Laummaunwai; Parichart Boueroy; Sukhonthip Khueangchaingkhwang; Benjamabhorn Pumhirunroj; Atchara Artchayasawat; Sirintip Boonjaraspinyo; Zhiliang Wu; Chariya Hahnvajanawong; Kulthida Vaeteewoottacharn; Sopit Wongkham
Journal:  Asian Pac J Cancer Prev       Date:  2017-03-01

Review 4.  Signaling control of the constitutive androstane receptor (CAR).

Authors:  Hui Yang; Hongbing Wang
Journal:  Protein Cell       Date:  2014-01-29       Impact factor: 14.870

  4 in total

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