Display options
Cite
Lee WW, Kim WS, Ahn G, et al. Separation of glycine-rich proteins from sea hare eggs and their anti-cancer activity against U937 leukemia cell line. EXCLI J. 2016;15:329-42doi: 10.17179/excli2016-293.
Lee, W. W., Kim, W. S., Ahn, G., Kim, K. N., Heo, S. J., Cho, M., Fernando, I. P., Kang, N., & Jeon, Y. J. (2016). Separation of glycine-rich proteins from sea hare eggs and their anti-cancer activity against U937 leukemia cell line. EXCLI journal, 15329-42. https://doi.org/10.17179/excli2016-293
Lee, Won Woo, et al. "Separation of glycine-rich proteins from sea hare eggs and their anti-cancer activity against U937 leukemia cell line." EXCLI journal vol. 15 (2016): 329-42. doi: https://doi.org/10.17179/excli2016-293
Lee WW, Kim WS, Ahn G, Kim KN, Heo SJ, Cho M, Fernando IP, Kang N, Jeon YJ. Separation of glycine-rich proteins from sea hare eggs and their anti-cancer activity against U937 leukemia cell line. EXCLI J. 2016 Jun 01;15:329-42. doi: 10.17179/excli2016-293. eCollection 2016. PMID: 27366143; PMCID: PMC4928013.
Copy Download .nbib Format: NLM
Share it on

EXCLI J. 2016 Jun 01;15:329-42. doi: 10.17179/excli2016-293. eCollection 2016.

Separation of glycine-rich proteins from sea hare eggs and their anti-cancer activity against U937 leukemia cell line.

EXCLI journal

Won Woo Lee, Won-Suck Kim, Ginnae Ahn, Kil-Nam Kim, Soo-Jin Heo, Moonjae Cho, I P Shanura Fernando, Nalae Kang, You-Jin Jeon

Affiliations

  1. School of Marine Biomedical Sciences, Jeju National University, Jeju 63243, Republic of Korea.
  2. College of Medical and Life Sciences, Silla University, Busan, 46958, Republic of Korea.
  3. Department of Marine Bio-Food Sciences, Chonnam National University, Yeosu 59626, Republic of Korea.
  4. Jeju center, Korea Basic Science Institute (KBSI), Jeju 690-140, Republic of Korea.
  5. Global Bioresources Research Center, Korea Institute of Ocean Science & Technology, Jeju, Republic of Korea.
  6. Department of Biochemistry, College of Medicine, Cheju National University, Jeju 63349, Republic of Korea.

PMID: 27366143 PMCID: PMC4928013 DOI: 10.17179/excli2016-293

Abstract

The present study was designed to investigate the anti-cancer effects of Sea hare eggs (SE) in U937 cells and its major active components. The aqueous extract of SE (ASE), which contained the highest protein content, dose-dependently inhibited the cancer cell's growth (IC50 value, 10.42 ± 0.5 µg/mL). Additionally, ASE markedly caused DNA damage by inducing apoptotic body formation, DNA fragmentation, and accumulation of sub-G1 DNA contents. ASE induced apoptosis by activating caspase-3 and 9 and poly (ADP-ribose) polymerase (PARP) by regulating the expression of Bcl-2/Bax. Moreover, among its molecular weight fractions, the > 30 kDa fraction showed the highest cell-growth-inhibitory effects, which was inhibited by heat treatment. Furthermore, the > 30 kDa fraction had markedly higher glycine content than the ASE. The presence of two protein bands at around 16 and 32 kDa was identified. In addition, two fractions, F1 and F2, were obtained using anion-exchange chromatography, with the F1 having an improved cell-growth-inhibitory effect than the > 30 kDa fraction. Taken together, these results suggest that the ASE contains glycine-rich proteins, including the active 16 and 32 kDa proteins, which account for its anti-cancer effects by inducing apoptosis via regulation of the mitochondrial pathway.

Keywords: anti-cancer effect; apoptosis; glycine-rich protein; mitochondrial pathway; sea hare egg (SE)

References

  1. J Neurochem. 1995 Jul;65(1):292-300 - PubMed
  2. Int Rev Cytol. 1980;68:251-306 - PubMed
  3. J Biol Chem. 1984 May 25;259(10):6579-85 - PubMed
  4. J Biol Chem. 1996 Jan 26;271(4):1841-4 - PubMed
  5. Science. 1997 Dec 12;278(5345):1966-8 - PubMed
  6. J Natl Cancer Inst. 1997 Dec 17;89(24):1881-6 - PubMed
  7. J Biol Chem. 1999 Jun 18;274(25):17484-90 - PubMed
  8. Trends Cardiovasc Med. 2005 Nov;15(8):283-90 - PubMed
  9. Trends Genet. 1999 Jun;15(6):229-35 - PubMed
  10. Nat Med. 2002 Mar;8(3):274-81 - PubMed
  11. J Nutr Biochem. 2008 Mar;19(3):166-74 - PubMed
  12. Annu Rev Cell Dev Biol. 1999;15:269-90 - PubMed
  13. Nature. 1995 Jul 6;376(6535):37-43 - PubMed
  14. Chem Pharm Bull (Tokyo). 1989 Nov;37(11):3050-3 - PubMed
  15. Cancer Lett. 2005 Nov 18;229(2):157-69 - PubMed
  16. J Med Food. 2005 Spring;8(1):69-77 - PubMed
  17. Apoptosis. 2008 Jan;13(1):177-86 - PubMed
  18. Food Chem Toxicol. 2010 Feb;48(2):536-8 - PubMed
  19. Chem Biol Interact. 2012 Aug 30;199(2):129-36 - PubMed
  20. Int J Biochem Cell Biol. 2013 Jan;45(1):123-9 - PubMed
  21. Science. 1997 Feb 21;275(5303):1132-6 - PubMed
  22. FEBS Lett. 1985 Jun 17;185(2):295-8 - PubMed
  23. Cancer Res. 1993 Sep 1;53(17):3976-85 - PubMed
  24. Cancer Lett. 2003 May 8;194(1):125-31 - PubMed
  25. J Biol Chem. 1995 May 19;270(20):11962-9 - PubMed
  26. Toxicol In Vitro. 2010 Sep;24(6):1648-54 - PubMed
  27. Microb Pathog. 2010 Nov;49(5):252-9 - PubMed
  28. Dev Comp Immunol. 1995 Jan-Feb;19(1):13-9 - PubMed
  29. Cancer Res. 1987 Nov 1;47(21):5649-53 - PubMed
  30. Arch Pharm Res. 1999 Oct;22(5):448-53 - PubMed
  31. J Immunol Methods. 1991 Jun 3;139(2):271-9 - PubMed
  32. Cytometry. 1995 Nov 1;21(3):275-83 - PubMed
  33. Mar Biotechnol (NY). 2011 Feb;13(1):66-73 - PubMed
  34. Nature. 1994 Sep 22;371(6495):346-7 - PubMed
  35. Cancer Chemother Pharmacol. 2004 Dec;54(6):562-72 - PubMed
  36. Int Immunopharmacol. 2007 Jan;7(1):36-45 - PubMed
  37. J Biomed Sci. 2007 Mar;14(2):223-32 - PubMed
  38. Cell Death Differ. 2001 Jul;8(7):715-24 - PubMed
  39. Free Radic Res. 2007 Jun;41(6):720-9 - PubMed
  40. Oncol Rep. 2005 Sep;14(3):789-96 - PubMed
  41. Protein J. 2011 Oct;30(7):509-19 - PubMed
  42. Anticancer Drugs. 2001 Nov;12(10):841-6 - PubMed
  43. Biol Pharm Bull. 1994 Aug;17(8):1144-6 - PubMed

Publication Types