Meme kanseri hücre dizisinde (MCF-7) selenyumun rolü

Meme kanseri dünyada sık görülen ölüm nedenleri arasında yer almaktadır, etyolojisinde genetik, endokrin ve çevresel faktörlerin rol aldığı bilinmektedir. Meme kanseri tedavisine yönelik yeni ajanların geliştirilmesi ya da varolan ilaçların etkinliğinin arttırılması için beslenmede takviye gıdaların alımı önem taşımaktadır. Deniz ürünleri, baklagiller, et, süt, kabuklu yemişler gibi bitkisel ve hayvansal gıdalardan alınan selenyumun kanser gelişiminin önlenmesi ya da baskılanmasında büyük öneme sahip olduğu bilinmektedir. Çalışmamızda, insan meme kanser hücre dizisine (MCF-7) 48 saat süreyle 200 nM selenyum uygulanarak tripan blue metodu ile hücre canlılığı, XTT ile hücre proliferasyonu, total antioksidan (TAS)-oksidan kapasite (TOS) ve oksidatif stres indeks (OSİ) değerleri ELİSA yöntemi ile analiz edilmiştir. Selenyum uygulanan grupta kontrol grubuna göre hücre canlılığı, proliferasyon, TAS, TOS değerlerinde istatistiksel olarak anlamlı olmamakla birlikte azalma tespit edilmiş, ayrıca OSİ değerinde artış olduğu görülmüştür. Sonuç olarak selenyumun doza, zamana bağlı olarak antioksidan veya sitotoksik etki gösterebileceği, farklı ajanlar ile kombinlenmesinin anti-kanser etkinliğinin araştırılmasında büyük önem taşıyabileceği düşünülmektedir.

Role of selenium in breast cancer cell line (MCF-7)

Breast cancer is among the common causes of death in the world, it is known that genetic, endocrine and environmental factors play a role in its etiology. The intake of supplements in nutrition is important for the development of new agents for breast cancer treatment or for increasing the effectiveness of existing drugs. Selenium intake from vegetable and animal foods such as seafood, legumes, meat, milk, and nuts has great importance in preventing or suppressing cancer development. In our study, 200 nM selenium was applied to a human breast cancer cell (MCF-7) line for 48 hours. Cell viability by trypan blue method, cell proliferation by XTT, total antioxidant (TAS)-oxidant capacity (TOS) and oxidative stress index (OSI) values were analyzed by ELISA method. A decrease was detected in cell viability, proliferation, TAS, TOS values and in the selenium applied group compared to the control group not to statistically significant. In addition an increase was evaluated OSI value. Consequently, it is thought that selenium may have antioxidant or cytotoxic effects depending on the dose and time, and its combination with different agents may be of great importance in the investigation of anti-cancer efficacy.

___

  • Ullah, F.M. (2019). Breast cancer: Current perspectives on the disease status. Adv Exp Med Biol, 1152, 51–64.
  • Ganz, P.A. & Pamela, G.J. (2015). Breast cancer survivorship: Where are we today? Adv Exp Med Biol, 862, 1–8.
  • Maughan, K.L., Lutterbie, M.A., Ham, P.S. (2010). Treatment of breast cancer. Am Fam Physician, 1(81), 1339–46.
  • Soyocak, A. & Koc, G. (2020). Effect of black grape extract on MMP-9 gene expression in breast cancer cells. Biological Diversity and Conservation, 13, 194–199.
  • Azizi, E., Shoeibi, S., Gabriele, L., G. & Oveisi, M.R. (2003). The inhibitory effects of ascorbic acid, α-tocopherol, and sodium selenite on proliferation of breast cancer cell lines. Iranian Journal of Pharmaceutical Research, 173–177.
  • Suzuki, M., Endo, M., Shinohara, F., Echigo, S. & Rikiishi, H. (2010). Differential apoptotic response of human cancer cells to organoselenium compounds. Cancer Chemother Pharmacol, 475–484.
  • Supuran, C.T., Casini, A. & Scozzafava, A. (2003). Protease inhibitors of the sulfonamidetype: Anticancer, antiinflammatory, and antiviral agents. Med Res Rev, 23, 535–558.
  • Papp, L.V., Lu, J., Holmgren, A. & Khanna, K. (2007). From selenium to selenoproteins: Synthesis, identity, and their role in human health. Antioxid Redox Signal, 9, 775–806.
  • Zimmerman, M.T., Bayse, C.A., Ramoutar, R.R. & Brumaghima, J.L. (2015). Sulfur and selenium antioxidants: Challenging radical scavenging mechanisms and developing structure-activity relationships based on metal binding. J Inorg Biochem, 145, 30–40.
  • Mueller, A.S., Mueller, K., Wolf, N.M. & Pallauf, J. (2009). Selenium and diabetes: An enigma? Free Radical Research, 43, 1029–1059.
  • Boasalis, M.G. (2008). The role of selenium in chronic disease. Nutrition in Clinical Practice, 23, 152–160.
  • Rocourt, C.R. & Cheng, W.H. (2013). Selenium supranutrition: Are the potential benefits of chemoprevention outweighed by the promotion of diabetes and insulin resistance? Nutrients, 1349–1365.
  • Rikiishi, H. (2007). Apoptotic cellular events for selenium compounds involved in cancer prevention. J Bioenerg Biomembr, 39(1), 91–98.
  • Gupta, R., Anwar, F. & Khosa, R.L. (2014). Cytotoxic activity of sulphonamide with selenium to decrease raised lipid profile in the treatment hepatocarcinogenesis. AJADD, 2(1), 14–21.
  • Berggren, M., Sittadjody, S., Song, Z., Samira, J.L., Burd, R. & Meuillet, E.J. (2009). Sodium selenite increases the activity of the tumor suppressor protein, pten in DU-145 prostate cancer cells. Nutr Cancer, 61, 322–331.
  • Whanger, P.D. (2001). Selenium and the brain: A review. Nutr Neurosci, 45(3), 164-178.
  • Pastacı Ozsobacı, N., Duzgun Ergun, D., Durmus, S., Tuncdemir, M., Uzun, H., Gelisgen, R. & Ozcelik, D. (2018). Selenium supplementation ameliorates electromagnetic field-induced oxidative stress in the HEK293 cells. J Trace Elem Med Biol, 50, 572-579.
  • Duzgun Ergun, D., Dursun, S., Pastaci Ozsobaci, N., Hatırnaz Ng, O., Naziroglu, M. & Ozcelik, D. (2020). The potential protective roles of zinc, selenium and glutathione on hypoxia induced TRPM2 channel activation in transfected HEK293 cells. J Recept Signal Transduct Res, 40(6), 521-530.
  • Guo, C.H., Hsia, F.S., Shih, M.Y., Hsieh, F.C. & Chen, P.C. (2015). Effects of selenium yeast on oxidative stress, growth inhibition, and apoptosis in human breast cancer cells. Int J Med Sci, 12(9), 748–758.
  • Cetin, S.E., Naziroglu, M., Cig, B., Ovey, I.S. & Kosar, P.A. (2017). Selenium potentiates the anticancer effect of cisplatin against oxidative stress and calcium ion signaling-induced intracellular toxicity in MCF-7 breast cancer cells: Involvement of the TRPV1 channel. J Recept Signal Transduct Res, 37, 84–93.
  • Alkhudhayri, A.A., Wahab, R., Siddiqui, M.A. & Ahmad, J. (2020). Selenium nanoparticles induce cytotoxicity and apoptosis in human breast cancer (MCF-7) and liver (HEPG2) cell lines. Nanoscience and Nanotechnology Letters, 12, 324–330.
  • Ganash, M.A. (2021). Anticancer potential of ascorbic acid and inorganic selenium on human breast cancer cell line MCF-7 and colon carcinoma HCT-116. J Can Res Ther, 17(1), 122-129.
  • Pi, J., Jin, H., Liu, R.Y., Song, B., Wu, Q. & Liu, L. (2012). Pathway of cytotoxicity induced by folic acid modified selenium nanoparticles in MCF-7 cells. Appl Microbiol Biotechnol, 97, 1051–1062.
  • Brozmanova, J., Manikova, D., Vlckova, V. & Chovanec, M. (2010). Selenium: A double-edged sword for defense and offence in cancer. Arch Toxicol, 919–938.
  • Zeng, H. & Combs, G.J. (2008). Selenium as an anticancer nutrient: Roles in cell proliferation and tumor cell invasion. J Nutr Biochem, 1–7.