Review: In Vitro Study Revealed Sugar As Anticancer Constituent

Öz

The majority of deaths among cancer patients are attributed to the metastatic spread of cancer cells to vital organs instead of primary tumor outgrowth. Plus, cancer therapeutics which focusing on conventional chemotherapy is often toxic not only to tumor cells but also to normal cells and caused their therapeutic use is limited. In this review, aberrant glycosylation is proposed to be a method of cancer diagnosis in order to identify cancer at its earliest and more treatable stage. Aberrant glycosylation is a universal feature of cancer cells. Glycosylation, the attachment of sugar moieties to protein, is a major form of post-translational modifi cation (PTM) that is observed in approximately half of all proteins. Certain glycan structures are well known markers for tumor progression and its availability and composition in the microenvironment may affect glycosylation of the cell. In order to understand the biological application of simple sugars as anticancer agents, it is vital to fundamentally investigate the relationship between simple sugars and cell proliferation using living cell lines in vitro. Various simple sugars have been studied previously in a number of cancer cell lines representing different evolutionary stages of cancer. It has been examined that there is a selective effect of individual simple sugars on the pattern of growth and metabolism of certain cell lines in tissue culture. The results from previous studies reported that certain simple sugars were able to alter the growth pattern and morphology of several cancer cell lines which indicate that sugars have antiproliferative effect on cancer cells.

Anahtar Kelimeler

• sugar,anticancer,in vitro

Review: In Vitro Study Revealed Sugar As Anticancer Constituent

Öz

Kanser hastalarında ölümlerin çoğunluğu, kanser hücrelerinin primer tümör gelişimi yerine hayati organlara yayılımı ile ilgilidir. Ayrıca, konvansiyonel kemoterapiye odaklanan kanser tedavileri, genellikle sadece tümör hücreleri için değil aynı zamanda normal hücrelere toksiktir ve terapötik kullanımının neden olduğu sınırlıdır. Bu derlemede, anormal glikozilasyon, kanseri en erken ve tedavisi mümkün olan aşamada tanımlamak için bir kanser tanısı yöntemi olarak önerilmiştir. Aşikâr glikosilasyon, kanser hücrelerinin evrensel bir özelliğidir. Glikosilasyon, şekere yarımların proteine bağlanması, tüm proteinlerin yaklaşık yarısında gözlemlenen post translasyonel modifi kasyonun (PTM) önemli bir şeklidir. Belirli glikan yapıları, tümör ilerlemesi için iyi bilinen belirteçlerdir ve mikro ortamdaki mevcut durumu ve bileşimi hücrenin glıkosilasyonunu etkileyebilir. Basit şekerlerin kanser önleyici ajanlar olarak biyolojik olarak uygulanmasını anlamak için basit şekerler ile hücre proliferasyonu arasındaki ilişkiyi in vitro canlı hücre dizileri kullanarak araştırmak hayati önem taşımaktadır. Çeşitli basit şekerler daha önce kanserin farklı evrim safhalarını temsil eden bir dizi kanser hücre dizisinde incelenmiştir. Doku kültüründe bazı hücre çizgilerinin büyüme ve metabolizma modelleri üzerinde bireysel basit şekerlerin seçici bir etkisi olduğu incelenmiştir. Önceki çalışmaların sonuçları, bazı basit şekerlerin, şekerlerin kanser hücreleri üzerinde antiproliferatif etkisi olduğuna işaret eden birkaç kanser hücre çizgisinin büyüme modelini ve morfolojisini değiştirebildiğini bildirmiştir.

Anahtar Kelimeler

• şeker,antikanser,in vitro

Kaynakça

1. 1. Yamashina, T., Ishihara, R., Nagai, K., Matsuura, N., Matsui, F., Ito, T., Fujii, M., Yamamoto, S., Hanaoka, N. & Takeuchi, Y. (2013). Long‑term outcome and metastatic risk after endoscopic resection of superficial esophageal squamous cell carcinoma. Am J Gastroenterol, 108, 544‑551.
2. 2. Häuselmann, I., & Borsig, L. (2014). Altered tumor-cell glycosylation promotes metastasis. Frontiers in oncology, 4, 28.
3. 3. Hakomori, S. (2001). Tumor-associated carbohydrate antigens defining tumor malignancy: Basis for development of anti-cancer vaccines. Adv Exp Med Biol, 491, 369–402.
4. 4. Chandrasekaran, E.V., Xue, J., Neelamegham, S., & Matta, K.L. (2006). The pattern of glycosyl- and sulfotransferase activities in cancer cell lines: A predictor of individual cancer-associated distinct carbohydrate structures for the structural identification of signature glycans. Carbohydr Res, 34, 983–994.
5. 5. Apweiler, R., Hermjakob, H., Sharon, N. (1999). On the frequency of protein glycosylation, as deduced from analysis of the SWISS-PROT database. Biochim Biophys Acta, 1473, 4–8.
6. 6. Fuster, M.M., & Esko, J.D. (2005). The sweet and sour of cancer: Glycans as novel therapeutic targets. Nat Rev Cancer, 5, 526–542.
7. 7. Berger, V., Perier, S., Pachiaudi, C., Normand, S., Louisot, P., & Martin, A. (1998). Dietary specific sugars for serum protein enzymaticglycosylation in man. Metabolism, 47, 1499-1503.
8. 8. Calvo, M. B., Figueroa, A., Pulido, E. G., Campelo, R. G., & Aparicio, L. A. (2010). Potential role of sugar transporters in cancer and their relationship with anticancer therapy. International journal of endocrinology.

9. 9. Delhotal, B., Lemonnier, F., Couturier, M., Wolfrom, C., Gautier, M., & Lemonnier, A. (1984). Comparative use of fructose and glucose in human liver and fibroblastic cell cultures. In Vitro, 20, 699-706.
10. 10. Wolfrom, C., Loriette, C., Polini, G., Delhotal, B., Lemonnier, F., & Gautier, M. (1983). Comparative effects of glucose and fructose on growth and morphological aspects of cultured skin fibroblasts. Exp Cell Res , 149, 535-546.
11. 11. Wolfrom, C., Kadhom, N., Raulin, J., Raynaud, N., & Gautier, M. (1994). Fructose-induced enhanced mitogenicity of diploid human cells: possible relationship with cell differentiation. In Vitro Cell Dev Biol Anim, 30A, 263-268.
12. 12. Tuccillo, F. M., de Laurentiis, A., Palmieri, C., Fiume, G., Bonelli, P., Borrelli, A., & Scala, G. (2014). Aberrant glycosylation as biomarker for cancer: focus on CD43. BioMed research international.
13. 13. Cox, R. P., & Gesner, B. M. (1965). Effect of simple sugars on the morphology and growth pattern of mammalian cell cultures. Proceedings of the National Academy of Sciences of the United States of America, 54(6), 1571.
14. 14. Monzavi-Karbassi, B., Hine, R. J., Stanley, J. S., Ramani, V. P., Carcel-Trullols, J., Whitehead, T. L. & Saha, R. (2010). Fructose as a carbon source induces an aggressive phenotype in MDA-MB-468 breast tumor cells. .International journal of oncology, 37(3), 615.
15. 15. Albini, A., Benelli, R., Noonan, D.M., & Brigati, C. (2004). The ‘chemoinvasionassay’: a tool to study tumor and endothelial cell invasion of basement membranes. Int J Dev Biol 48, 563-571.
16. 16. Yamaguchi, F., Takata, M., Kamitori, K., Nonaka, M., Dong, Y., Sui, L., & Tokuda, M. (2008). Rare sugar D-allose induces specific up-regulation of TXNIP and subsequent G1 cell cycle arrest in hepatocellular carcinoma cells by stabilization of p27kip1. International journal of oncology, 32(2), 377-386.
17. 17. Sui, L., Dong, Y., Watanabe, Y., Yamaguchi, F., Hatano, N., Tsukamoto, I. & Tokuda, M. (2005). The inhibitory effect and possible mechanisms of D-allose on cancer cell proliferation. International journal of oncology, 27(4), 907-912.
18. 18. Izumori, K. (2002). Bioproduction strategies for rare hexose sugars. Naturwissenschaften 89, 120-124.
19. 19. Bekesi, J. G., Molnar, Z., & Winzler, R. J. (1969). Inhibitory effect of D-glucosamine and other sugar analogs on the viability and transplantability of ascites tumor cells. Cancer research, 29(2), 353-359.
20. 20. Fare, G., Sammons, D. C. H., Seabourne, F. A., & Woodhouse, D. L. (1967). Lethal Action of Sugars on Ascites Tumor Cells in vitro. Nature, 214, 308-309.
21. 21. Baba, T., Yoshida, T., Yoshida, T. & Cohen, S. (1979). Suppression of cell-mediated immune reactions by monosaccharides. J Immunol, 122, 838-841.
22. 22. Stutman, O., Dien, P., Wisun, R.E. & Lattime, E.C. (1980). Natural cytotoxic cells against solid tumors in mice: blocking of cytotoxicity by D-mannose. Proc Natl Acad Sci USA, 77, 2895-2898.