Proteomic Analysis of Tumor Tissue after Treatment with Ascorbic Acid
Tumor cells have an invasive and metastatic phenotype
that is the main cause of death for cancer patients. Tumor
establishment and penetration consists of a series of complex
processes involving multiple changes in gene expression. In this study,
intraperitoneal administration of a high concentration of ascorbic acid
inhibited tumor establishment and decreased tumor mass in BALB/C
mice implanted with S-180 sarcoma cancer cells. To identify proteins
involved in the ascorbic acid-mediated inhibition of tumor
progression, changes in the tumor proteome associated with ascorbic
acid treatment of BALB/C mice implanted with S-180 were
investigated using two-dimensional gel electrophoresis and mass
spectrometry. Twenty protein spots were identified whose expression
was different between control and ascorbic acid treatment groups.
[1] S. J. Padayatty, H. Sun, Y. Wang, H. D. Riordan, S. M. Hewitt, A. Katz, R.
A. Wesley, and M. Levine, "Vitamin C pharmacokinetics: implications
for oral and intravenous use," Ann Intern Med, vol. 140, pp. 533-537,
2004.
[2] S. Bram, P. Froussard, M. Guichard, C. Jasmin, Y. Augery, F.
Sinoussi-Barre, and W. Wray, "Ascorbic acid preferential toxicity for
malignant melanoma cells," Nature vol. 284, pp. 629-631, 1980.
[3] G. Bruchelt, L. Baader, A. G. Reith, N. L. Holger, S. Gebhardt, and D.
Niethammer, "Rationale for the use of ascorbic acid in neuroblastoma
therapy," Human Neuroblastoma. Newark: Harwood Academic
Publishers, pp. 34-40, 1993.
[4] S. Fujinaga, H. Sakagami, N. Kuribayashi, H. Takahashi, Y. Amano, T.
Sakagami, and M. Takeda, "Possible role of hydrogen peroxide in
apoptosis induction by ascorbic acid in human myelogenous leukemic cell
lines," Showa Univ Med Sci, vol. 6, pp. 135-144, 1994.
[5] V. De Laurenzi, G. Melino, I. Savini, M. Annicchiarico-Petruzzelli, A.
Finazzi-Agro, and L. Avigliano, "Cell death by oxidative stress and
ascorbic acid regeneration in human neuroectodermal cell lines," Eur J
Cancer, vol 31A, pp. 463-466, 1995.
[6] C. H. Park, B. F. Kimler, D. Bodensteiner, S. R. Lynch, and R. S.
Hassanein, "In vitro growth modulation by L-ascorbic acid of
colony-forming cells from bone marrow of patients with myelodysplastic
syndromes," Cancer Res, vol. 52, pp. 4458-4466, 1992.
[7] C. H. Park, "Biological nature of the effect of ascorbic acids on the growth
of human leukemic cells," Cancer Res, vol. 45, pp. 3969-3973, 1985.
[8] S. Park, S. S. Han, C. H. Park, E. R. Hahm, S. J. Lee, H. K. Park, S. H. Lee,
W. S. Kim, C. W. Jung, K. Park, H. D. Riordan, B. F. Kimler, K. Kim, and
J. H. Lee, "L-Ascorbic acid induces apoptosis in acute myeloid leukemia
cells via hydrogen peroxidemediated mechanisms," Int J Biochem Cell
Biol, vol. 36, pp. 2180-2195, 2004.
[9] I. J. Fidler, "Critical determinants of cancer metastasis: rationale for
therapy," Cancer Chemother Pharmacol, vol. 43, pp. S3-10, 1999.
[10] P. Mignatti and D. B. Rifkin, "Biology and biochemistry of proteinases in
tumor invasion," Physiol Rev, vol. 73, pp. 161-195, 1993.
[11] M. Rath and L. Pauling, "Plasmin-induced proteolysis and the role of
apoprotein(a), lysine and synthetic analogs," Orthomol Med, vol. 7, pp.
17-23, 1992.
[12] M. W. Roomi, N. W. Roomi, V. Ivanov, T. Kalinovsky, A. Niedzwiecki,
and M. Rath, "Modulation of N-methyl-N-nitrosourea induced mammary
tumors in Sprague-Dawley rats by combination of lysine, proline,
arginine, ascorbic acid and green tea extract," Breast Cancer Res, vol. 7,
pp. R291-295, 2005.
[13] E. C. Kohn, "Development and prevention of metastasis," Anticancer Res,
vol. 13, pp. 2553-2559, 1993.
[14] E. Wybieralska, M. Koza, J. Sroka, J. Czyz, and Z. Madeja, "Ascorbic
acid inhibits the migration of Walker 256 carcinosarcoma cells," Cell Mol
Biol Lett, vol. 13, pp. 103-111, 2008.
[15] G. G. Meadows, H. F. Pierson, and R. M. Abdallah, "Ascorbate in the
treatment of experimental transplanted melanoma," Am J Clin Nutr, vol.
54, pp. 1284S-1291S, 1991.
[16] H. S. Taper, J. M. Jamison, J. Gilloteaux, J. L. Summers, and P. B.
Calderon, "Inhibition of the development of metastases by dietary vitamin
C:K3 combination," Life Sci, vol. 75, pp. 955-967, 2004.
[1] S. J. Padayatty, H. Sun, Y. Wang, H. D. Riordan, S. M. Hewitt, A. Katz, R.
A. Wesley, and M. Levine, "Vitamin C pharmacokinetics: implications
for oral and intravenous use," Ann Intern Med, vol. 140, pp. 533-537,
2004.
[2] S. Bram, P. Froussard, M. Guichard, C. Jasmin, Y. Augery, F.
Sinoussi-Barre, and W. Wray, "Ascorbic acid preferential toxicity for
malignant melanoma cells," Nature vol. 284, pp. 629-631, 1980.
[3] G. Bruchelt, L. Baader, A. G. Reith, N. L. Holger, S. Gebhardt, and D.
Niethammer, "Rationale for the use of ascorbic acid in neuroblastoma
therapy," Human Neuroblastoma. Newark: Harwood Academic
Publishers, pp. 34-40, 1993.
[4] S. Fujinaga, H. Sakagami, N. Kuribayashi, H. Takahashi, Y. Amano, T.
Sakagami, and M. Takeda, "Possible role of hydrogen peroxide in
apoptosis induction by ascorbic acid in human myelogenous leukemic cell
lines," Showa Univ Med Sci, vol. 6, pp. 135-144, 1994.
[5] V. De Laurenzi, G. Melino, I. Savini, M. Annicchiarico-Petruzzelli, A.
Finazzi-Agro, and L. Avigliano, "Cell death by oxidative stress and
ascorbic acid regeneration in human neuroectodermal cell lines," Eur J
Cancer, vol 31A, pp. 463-466, 1995.
[6] C. H. Park, B. F. Kimler, D. Bodensteiner, S. R. Lynch, and R. S.
Hassanein, "In vitro growth modulation by L-ascorbic acid of
colony-forming cells from bone marrow of patients with myelodysplastic
syndromes," Cancer Res, vol. 52, pp. 4458-4466, 1992.
[7] C. H. Park, "Biological nature of the effect of ascorbic acids on the growth
of human leukemic cells," Cancer Res, vol. 45, pp. 3969-3973, 1985.
[8] S. Park, S. S. Han, C. H. Park, E. R. Hahm, S. J. Lee, H. K. Park, S. H. Lee,
W. S. Kim, C. W. Jung, K. Park, H. D. Riordan, B. F. Kimler, K. Kim, and
J. H. Lee, "L-Ascorbic acid induces apoptosis in acute myeloid leukemia
cells via hydrogen peroxidemediated mechanisms," Int J Biochem Cell
Biol, vol. 36, pp. 2180-2195, 2004.
[9] I. J. Fidler, "Critical determinants of cancer metastasis: rationale for
therapy," Cancer Chemother Pharmacol, vol. 43, pp. S3-10, 1999.
[10] P. Mignatti and D. B. Rifkin, "Biology and biochemistry of proteinases in
tumor invasion," Physiol Rev, vol. 73, pp. 161-195, 1993.
[11] M. Rath and L. Pauling, "Plasmin-induced proteolysis and the role of
apoprotein(a), lysine and synthetic analogs," Orthomol Med, vol. 7, pp.
17-23, 1992.
[12] M. W. Roomi, N. W. Roomi, V. Ivanov, T. Kalinovsky, A. Niedzwiecki,
and M. Rath, "Modulation of N-methyl-N-nitrosourea induced mammary
tumors in Sprague-Dawley rats by combination of lysine, proline,
arginine, ascorbic acid and green tea extract," Breast Cancer Res, vol. 7,
pp. R291-295, 2005.
[13] E. C. Kohn, "Development and prevention of metastasis," Anticancer Res,
vol. 13, pp. 2553-2559, 1993.
[14] E. Wybieralska, M. Koza, J. Sroka, J. Czyz, and Z. Madeja, "Ascorbic
acid inhibits the migration of Walker 256 carcinosarcoma cells," Cell Mol
Biol Lett, vol. 13, pp. 103-111, 2008.
[15] G. G. Meadows, H. F. Pierson, and R. M. Abdallah, "Ascorbate in the
treatment of experimental transplanted melanoma," Am J Clin Nutr, vol.
54, pp. 1284S-1291S, 1991.
[16] H. S. Taper, J. M. Jamison, J. Gilloteaux, J. L. Summers, and P. B.
Calderon, "Inhibition of the development of metastases by dietary vitamin
C:K3 combination," Life Sci, vol. 75, pp. 955-967, 2004.
@article{"International Journal of Medical, Medicine and Health Sciences:62409", author = "Seyeon Park and Mi Jang", title = "Proteomic Analysis of Tumor Tissue after Treatment with Ascorbic Acid", abstract = "Tumor cells have an invasive and metastatic phenotype
that is the main cause of death for cancer patients. Tumor
establishment and penetration consists of a series of complex
processes involving multiple changes in gene expression. In this study,
intraperitoneal administration of a high concentration of ascorbic acid
inhibited tumor establishment and decreased tumor mass in BALB/C
mice implanted with S-180 sarcoma cancer cells. To identify proteins
involved in the ascorbic acid-mediated inhibition of tumor
progression, changes in the tumor proteome associated with ascorbic
acid treatment of BALB/C mice implanted with S-180 were
investigated using two-dimensional gel electrophoresis and mass
spectrometry. Twenty protein spots were identified whose expression
was different between control and ascorbic acid treatment groups.", keywords = "Ascorbic acid, Proteomic analysis, S-180 implantedBALB/C mouse", volume = "4", number = "4", pages = "156-4", }
