ECE2016 Eposter Presentations Endocrine tumours and neoplasia (68 abstracts)
Potential role of the adrenolitic drug mitotane in the treatment of hepatocarcinoma (HCC): effect on cell proliferation in HCC cell lines
Claudia Pivonello 1 , Donatella Paola Provvisiero 1 , Mariarosaria Negri 1 , Gilda Di Gennaro 1 , Cristina De Angelis 2 , Chiara Simeoli 1 , Roberta Patalano 1 , Maria Cristina De Martino 1 , Annamaria Colao 1 & Rosario Pivonello 1
1Department of Clinical Medicine and Surgery, University of Naples Federico Ii, Naples, Italy; 2Ios & Coleman Medicina Futura Medical Center, Centro Direzionale, Naples, Italy.
HCC is one of the most common malignancies worldwide. Local approaches are generally preferred for patients whose disease is restricted to the liver. In patients with extrahepatic disease systemic therapy can be considered. Chemotherapy did not demonstrate convincing survival advantages in several trails for HCC patients. Presently, the kinase inhibitor sorafenib is the only approved systemic target therapy for the treatment of advanced HCC. Mitotane (dichlorodiphenildichloroethane or o,p’DDD), a chemotherapeutic agent, is the only drug approved for the treatment of advanced adrenocortical cancer (ACC) but no data are available concerning its cytotoxic role in different cancers, including HCC. The aim of this study was to evaluate the effect of mitotane on cell proliferation in HCC cell lines. HepG2, HuH-7, JHH-6, PLC/PRF/5 HCC cell lines, and H295R, ACC cell line, were used for the study. DNA assay was conduced to evaluate the rate of inhibition after 6 days of treatment with mitotane in a concentration ranging between 10−6 and 10−5 M, beneath the plasma mitotane levels achieved by ACC patients. Western blot analysis for PARP cleavage was performed to evaluate apoptosis. Mitotane was able to inhibit cell proliferation in a dose-dependent manner with a maximal effect of 54%, at 10−5 M (P<0.001) and minimum effect of 35%, at 5*10−6 M (P<0.01) in PLC/PRF/5; maximal effect of 49%, at 10−5 M (P<0.001) and minimum effect at 32%, at 7.5*10−6 M (P<0.001) in JHH-6; maximal effect of 45.5%, at 10−5 M (P<0.001) and minimum effect of 20%, at 5*10−6 M (P<0.001) in HuH7; maximal effect of 36%, at 10−5 M (P<0.001) and minimum effect of 15.4%, at 5*10−6 M (P<0.01) in HepG2. In H295R, that were used as control, maximal effect was 82%, at 10−5 M (P<0.001) and minimum effect was 52%, at 5*10−6 M (P<0.001). In each HCC cell line mitotane induced apoptosis as demonstrated by PARP cleavage after 2 h of treatment. In conclusion, these preliminary data demonstrated the in vitro antiproliferative role of mitotane in HCC cell lines suggesting its potential use in the treatment of HCC.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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