Tumor growth effects of rapamycin on human biliary tract cancer cells

被引:3
作者
Heuer, Matthias [1 ]
Dreger, Nici M. [1 ]
Cicinnati, Vito R. [2 ]
Fingas, Christian [1 ,3 ]
Juntermanns, Benjamin [1 ]
Paul, Andreas [1 ]
Kaiser, Gernot M. [1 ]
机构
[1] Univ Hosp Essen, Dept Gen Visceral & Transplantat Surg, D-45122 Essen, Germany
[2] Univ Hosp, Dept Gastroenterol & Hepatol, Essen, Germany
[3] Mayo Clin, Div Gastroenterol & Hepatol, Rochester, MN USA
关键词
Anti-tumor effect; Biliary tract carcinoma; Liver transplantation; Rapamycin; LIVER-TRANSPLANTATION; HEPATOCELLULAR-CARCINOMA; CYCLOSPORINE; CHOLANGIOCARCINOMA; SIROLIMUS; RECURRENCE; FKBP12; TARGET; TOR;
D O I
10.1186/2047-783X-17-20
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Background: Liver transplantation is an important treatment option for patients with liver-originated tumors including biliary tract carcinomas (BTCs). Post-transplant tumor recurrence remains a limiting factor for long-term survival. The mammalian target of rapamycin-targeting immunosuppressive drug rapamycin could be helpful in lowering BTC recurrence rates. Therein, we investigated the antiproliferative effect of rapamycin on BTC cells and compared it with standard immunosuppressants. Methods: We investigated two human BTC cell lines. We performed cell cycle and proliferation analyses after treatment with different doses of rapamycin and the standard immunosuppressants, cyclosporine A and tacrolimus. Results: Rapamycin inhibited the growth of two BTC cell lines in vitro. By contrast, an increase in cell growth was observed among the cells treated with the standard immunosuppressants. Conclusions: These results support the hypothesis that rapamycin inhibits BTC cell proliferation and thus might be the preferred immunosuppressant for patients after a liver transplantation because of BTC.
引用
收藏
页数:6
相关论文
共 31 条
[1]  
[Anonymous], TRANSPLANT MEDICINE
[2]   The TOR pathway: A target for cancer therapy [J].
Bjornsti, MA ;
Houghton, PJ .
NATURE REVIEWS CANCER, 2004, 4 (05) :335-348
[3]   Malignancy after transplantation [J].
Buell, JF ;
Gross, TG ;
Woodle, ES .
TRANSPLANTATION, 2005, 80 (02) :S254-S264
[4]   Mechanisms of mTOR inhibitor resistance in cancer therapy [J].
Carew, Jennifer S. ;
Kelly, Kevin R. ;
Nawrocki, Steffan T. .
TARGETED ONCOLOGY, 2011, 6 (01) :17-27
[5]   Toward the definition of immunosuppressive regimens with antitumor activity [J].
Casadio, F ;
Croci, S ;
Grigioni, AD ;
Corti, B ;
Grigioni, WF ;
Landuzzi, L ;
Lollini, PL .
TRANSPLANTATION PROCEEDINGS, 2005, 37 (05) :2144-2147
[6]   Rapamycin Inhibits Cholangiocyte Regeneration by Blocking Interleukin-6-Induced Activation of Signal Transducer and Activator of Transcription 3 After Liver Transplantation [J].
Chen, Li-Ping ;
Zhang, Qi-Hao ;
Chen, Geng ;
Qian, Ye-Yong ;
Shi, Bing-Yi ;
Dong, Jia-Hong .
LIVER TRANSPLANTATION, 2010, 16 (02) :204-214
[7]   A PUTATIVE SIROLIMUS (RAPAMYCIN) EFFECTOR PROTEIN [J].
CHEN, YQ ;
CHEN, HH ;
RHOAD, AE ;
WARNER, L ;
CAGGIANO, TJ ;
FAILLI, A ;
ZHANG, HZ ;
HSIAO, CL ;
NAKANISHI, K ;
MOLNARKIMBER, KL .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1994, 203 (01) :1-7
[8]   RAPT1, A MAMMALIAN HOMOLOG OF YEAST TOR, INTERACTS WITH THE FKBP12 RAPAMYCIN COMPLEX [J].
CHIU, MI ;
KATZ, H ;
BERLIN, V .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (26) :12574-12578
[9]   Complete remission of postransplant lung metastases from hepatocellular carcinoma under therapy with sirolimus and mycophenolate mofetil [J].
Elsharkawi, M ;
Staib, L ;
Henne-Bruns, D ;
Mayer, J .
TRANSPLANTATION, 2005, 79 (07) :855-857
[10]  
Francis H, 2010, AM J PHYSIOL-GASTR L, V299, P1