Abstract
Amaç:
Yaptığımız çalışmada oral antidiyabetik olarak kullanılan pioglitazonun, 3
farklı dozda ve 5 farklı saat aralığında karaciğer kanseri modeli hücre hattı
(Hep3B) üzerinde hücre proliferasyonu üzerine etkisi araştırıldı.
Gereç ve Yöntem:
Pioglitazonun çalışmada kullanılan hepatosellüler kanser hücre hattı modeli
olan Hep3B hücre hattı üzerinde sitotoksik etkisi 3, 6, 24, 48 ve 72 saatlerde,
1, 2.5 ve 5 mM arasında değişen 3 farklı dozda uygulanarak MTT testi yapıldı.
Sonuçlar istatistiksel olarak analiz edildi ve yorumlandı. Pioglitazonun doza
ve zamana spesifik hücre proliferasyonu üzerine etkisi belirlendi.
Bulgular: Pioglitazon
karaciğer kanseri hücre hattı (Hep3B)’nda hücre proliferasyonu üzerine tüm saat
ve dozlarda herhangi bir etkisi görülmedi. 3 saat bekleme süresinde 1mM da ve
48 saatte 5 mM dozlarda hücre proliferasyonundaki azalış istatistiksel olarak
anlamlı değildir.
Sonuç: Bu
çalışmada pioglitazonun Karaciğer kanserinden korunmada ya da var olan kanser
hücrelerinde hücre canlılığı üzerine etkisi araştırıldı. Pioglitazon hepatoselüler
karsinoma hücre hattına (Hep3B) hücre canlılığına etkisi MTT testi ile
belirlenmiştir. Farklı zaman aralıklarında ve farklı dozlarda uygulanmış ve
hücre canlılığı üzerindeki etkisinin olmadığı belirlendi. Uygulamada bazı doz
ve saat aralıklarında gözlenen azalmanın istatistiksel olarak anlamı yoktu.
References
- Erstad, Derek J., and Kenneth K. Tanabe. "Hepatocellular carcinoma: early-stage management challenges." Journal of Hepatocellular Carcinoma 4 (2017): 81.
- El-Serag, H. B. (2012). Epidemiology of viral hepatitis and hepatocellular carcinoma. Gastroenterology, 142(6), 1264-1273.
- Guzman, G., Brunt, E. M., Petrovic, L. M., Chejfec, G., Layden, T. J., & Cotler, S. J. (2008). Does nonalcoholic fatty liver disease predispose patients to hepatocellular carcinoma in the absence of cirrhosis?. Archives of pathology & laboratory medicine, 132(11), 1761-1766.
- Tanaka, K., Tsuji, I., Tamakoshi, A., Matsuo, K., Ito, H., Wakai, K., ... & Tsugane, S. (2012). Obesity and liver cancer risk: an evaluation based on a systematic review of epidemiologic evidence among the Japanese population. Japanese journal of clinical oncology, 42(3), 212-221.
- Sirtori, C. R., & Pasik, C. (1994). Re-evaluation of a biguanide, metformin: mechanism of action and tolerability. Pharmacological research, 30(3), 187-228.
- Davila JA, Morgan RO, Shaib Y, McGlynn KA, El-Serag HB. Diabetes increases the risk of hepatocellular carcinoma in the United States: a population based case–control study. Gut 2005; 54: 533–9
- El-Serag HB, Tran T, Everhart JE. Diabetes increases the risk of chronic liver disease and hepatocellular carcinoma. Gastroenterology 2004; 126: 460–8.
- Wang Z, Olumi AF. Diabetes, growth hormone-insulin-like growth factor pathways and association to benign prostatic hyperplasia. Differentiation. 2011; 82(4-5):261-271.
- Zakikhani M, Dowling R, Fantus IG, Sonenberg N, Pollak M. Metformin is an AMP kinase-dependent growth inhibitor for breast cancer cells. Cancer Res. 2006; 66(21):10269-73.
Abstract
Objective: In this study, the effects of the oral antidiabetic pioglitazone on the
cell proliferation of hepatocarcinoma cell line (Hep3B) at 3 different doses
and 5 different time intervals was investigated.
Material and Methods: Pioglitazone was applied to the Hep3B cells, which was the
hepatocellular cancer cell line used in the study, at 1, 2.5 and 5 Mm doses and
for 3, 6, 24, 48 and 72 hours, and the MTT test was performed. The results were
statistically analyzed, interpreted and the dose and time dependent effect of
pioglitazone on the cell proliferation was determined.
Results: Pioglitazone showed
no effect on the cell proliferation of liver cancer cell line (Hep3B) at all doses
and time intervals. Even some decrease in cell proliferation was seen in 1mM
dose for 3 hours group and 5Mm dose for 48 hours groups, the differences were
not statistically significant.
Conclusion: In this study, we investigated the effect of pioglitazone on cell
viability in cancer cells that are present in the liver from cancer prevention.
The effect of the pioglitazone on the cell viability in hepatocellular
carcinoma cell line (Hep3B) was determined by MTT assay. It was administered at
different time intervals and at different doses and was found to have no effect
on cell viability. In practice, the decrease observed at some dose and time
intervals was not statistically significant.
Keywords
References
- Erstad, Derek J., and Kenneth K. Tanabe. "Hepatocellular carcinoma: early-stage management challenges." Journal of Hepatocellular Carcinoma 4 (2017): 81.
- El-Serag, H. B. (2012). Epidemiology of viral hepatitis and hepatocellular carcinoma. Gastroenterology, 142(6), 1264-1273.
- Guzman, G., Brunt, E. M., Petrovic, L. M., Chejfec, G., Layden, T. J., & Cotler, S. J. (2008). Does nonalcoholic fatty liver disease predispose patients to hepatocellular carcinoma in the absence of cirrhosis?. Archives of pathology & laboratory medicine, 132(11), 1761-1766.
- Tanaka, K., Tsuji, I., Tamakoshi, A., Matsuo, K., Ito, H., Wakai, K., ... & Tsugane, S. (2012). Obesity and liver cancer risk: an evaluation based on a systematic review of epidemiologic evidence among the Japanese population. Japanese journal of clinical oncology, 42(3), 212-221.
- Sirtori, C. R., & Pasik, C. (1994). Re-evaluation of a biguanide, metformin: mechanism of action and tolerability. Pharmacological research, 30(3), 187-228.
- Davila JA, Morgan RO, Shaib Y, McGlynn KA, El-Serag HB. Diabetes increases the risk of hepatocellular carcinoma in the United States: a population based case–control study. Gut 2005; 54: 533–9
- El-Serag HB, Tran T, Everhart JE. Diabetes increases the risk of chronic liver disease and hepatocellular carcinoma. Gastroenterology 2004; 126: 460–8.
- Wang Z, Olumi AF. Diabetes, growth hormone-insulin-like growth factor pathways and association to benign prostatic hyperplasia. Differentiation. 2011; 82(4-5):261-271.
- Zakikhani M, Dowling R, Fantus IG, Sonenberg N, Pollak M. Metformin is an AMP kinase-dependent growth inhibitor for breast cancer cells. Cancer Res. 2006; 66(21):10269-73.
Details
| Subjects | Clinical Sciences |
|---|---|
| Journal Section | RESEARCH ARTICLE |
| Authors | |
| Publication Date | December 18, 2017 |
| Published in Issue | Year 2017 Volume: 1 Issue: 3 |
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