Effect of tumour necrosis factor-α and irradiation alone or in combination on the viability of hepatocellular and biliary adenocarcinoma cell linesin vitro
| Autor: | Hans Christiansen, Clemens F. Hess, Bernhard Saile, Margret Rave-Fränk, Giuliano Ramadori, Blendi Qesaraku, Joszef Dudas |
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| Rok vydání: | 2009 |
| Předmět: |
Pathology
medicine.medical_specialty Blotting Western Antineoplastic Agents Apoptosis Adenocarcinoma In Vitro Techniques Biology chemistry.chemical_compound In vivo Cell Line Tumor medicine Humans Viability assay Tumor Stem Cell Assay DNA Primers Hepatology Reverse Transcriptase Polymerase Chain Reaction Tumor Necrosis Factor-alpha Liver Neoplasms Trypan Blue medicine.disease Blot Biliary Tract Neoplasms chemistry Cell culture Cancer research Trypan blue Tumor necrosis factor alpha |
| Zdroj: | Liver International. 29:910-921 |
| ISSN: | 1478-3231 1478-3223 |
| Popis: | Background Tumour necrosis factor alpha (TNF-alpha) may exhibit antitumoral activity and can influence the reaction of both tumour and normal tissue to radiation. Aims To test the effect of TNF-alpha and/or irradiation on hepatocellular (HepG2, Hep3B, Sk-Hep1, HuH7) and cholangiocellular (Sk-chA1, Mz-chA1) tumour cell lines. Methods Colony formation, apoptosis analysis and trypan blue exclusion were used to assess cell viability. Doses of radiation (2-25 Gy) and TNF-alpha (100-50,000 U) as well as their respective sequencing were varied (24 and 12 h before and 6 h after). The expression of TNF-alpha and TNF receptors 1/2 was determined using real-time polymerase chain reaction and IkappaBalpha protein expression was detected by Western blot. Results Sole irradiation induced a reduction in colony formation in all cell lines and sole TNF-alpha in HepG2 and Sk-chA1 cells only. No difference in apoptosis induction after TNF-alpha or irradiation was observed. Cellular death induced by the combination of TNF-alpha and radiation was not superior to the use of any of the two agents alone. All cell lines revealed that radiation induced upregulation of TNF-alpha whereas the extent of TNF receptor-specific transcription did not change. Furthermore, radiation-induced changes in IkappaBalpha expression were not detectable. Conclusions Our data suggest that both TNF-alpha and radiation may be treatment options for hepatocellular and cholangiocellular carcinomas. Because TNF-alpha and radiation do not interact in terms of radiosensitization, anti-TNF-alpha treatment may have the potential to protect against hepatocellular injury after abdominal irradiation. However, further in vivo studies are needed to confirm that anti-TNF-alpha treatment does not compromise tumour control and actually attenuates radiation-induced liver injury. |
| Databáze: | OpenAIRE |
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