213
Views
23
CrossRef citations to date
0
Altmetric
Original Articles

Apoptosis Induced by Niacin-related Compounds in HL-60 Cells

, , &
Pages 2351-2356 | Received 06 Jul 1998, Accepted 14 Aug 1998, Published online: 22 May 2014

  • 1) Steller, H., Mechanisms and genes of cellular suicide. Science, 267, 1445-1449 (1995).
  • 2) Martin, S. J., and Green, D. R., Protease activation during apoptosis: Death by a thousand cuts? Cell, 82, 349-352 (1995).
  • 3) Lazebnik, Y. A., Kaufmann, S. H., Desnoyers, S., Poirier, G. G., and Earnshaw, W. C., Cleavage of poly(ADP-ribose) polymerase by a proteinase with properties like ICE. Nature, 371, 346-347 (1994).
  • 4) Shiokawa, D., Maruta, H., and Tanuma, S., Inhibitors of poly(ADP-ribose) polymerase suppress nuclear fragmentation and apoptotic-body formation during apoptosis in HL-60 cells. FEBS Lett., 413, 99-103 (1997).
  • 5) Kuo, M.-L., Chau, Y.-P., Wang, J.-H., and Shiah, S.-G., Inhibitors of poly(ADP-ribose) polymerase block nitric oxide-induced apoptosis but not differentiation in human leukemia HL-60 cells. Biochem. Biophys. Res. Commun., 219, 502-508 (1996).
  • 6) Nosseri, C., Coppola, S., and Ghibelli, L., Possible involvement of poly(ADP-ribosyl) polymerase in triggering stress-induced apoptosis. Exp. Cell Res., 212, 367-373 (1994).
  • . 1989.
  • . 1992.
  • 9) Wang, Z.-Q., Auer, B., Sting, L., Berghammer, H., Haidacher, D., Schweiger, M., and Wagner, E. F., Mice lacking ADPRT and poly(ADP-ribosyl)ation develop normally but are susceptible to skin disease. Genes Dev., 9, 509-520 (1995).
  • 10) Wang, Z.-Q., Sting, L., Morrison, C., Jantsch, M., Los, M., Schulze-Ostchoff, K., and Wanger, E. F., PARP is important for genomic stability but dispensable in apoptosis. Genes Dev., 11, 2347-2358 (1997).
  • 11) de Murcia, J. M., Niedergang, C., Trucco, C., Ricoul, M., Dutrillaux, B., Mark, M., Oliver, F. J., Masson, M., Dierich, A., LeMeur, M., Walztinger, C., Chambon, P., and de Murcia, G., Requirement of poly(ADP-ribose) polymerase in recovery from DNA damage in mice and in cells. Proc. Natl. Acad. Sci. USA, 94, 7303-7307 (1997).
  • 12) Svedmyr, N., Harthon, L., and Lundholm, L., The relationship between the plasma concentration of free nicotinic acid and some of its pharmacologic effects in man. Clin. Pharmacol. Ther., 10, 559-570 (1969).
  • 13) Dulin, W. E., and Wyse, M., Reversal of streptozotocin diabetes with nicotinamide. Proc. Soc. Exp. Biol. Med., 130, 992-994 (1969).
  • 14) Ogata, S., Okumura, K., and Taguchi, H., The effects of niacin on DNA repair after N-methyl-N′-nitro-N-nitrosoguanidine treatment in normal human lymphocytes. Biosci. Biotechnol. Biochem., 61, 2116-2118 (1997).
  • 15) Nicoletti, I., Migliorati, G., Pagliacci, M. C., Grignani, F., and Riccardi, C., A rapid and simple method for measuring thymocyte apoptosis by propidium iodide staining and flow cytometry. J. Immunol. Methods, 139, 271-279 (1991).
  • 16) Evans, G. W., and Johnson, E. C., Growth stimulating effect of picolinic acid added to rat diets. Proc. Soc. Exp. Biol. Med., 165, 457-461 (1980).
  • 17) Warth, A. D., Determination of dipicolinic acid in bacterial spores by derivative spectroscopy, Anal. Biochem., 130, 502-505 (1983).
  • 18) Kristen, S. K., Sherril, L. G., and P. Richard, V., Iron deprivation inhibits cyclin-dependent kinase activity and decrease cyclin D/CDK4 protein levels in asynchronous MDA-MB-453 human breast cancer cells. Exp. Cell Res., 229, 60-68 (1996).
  • 19) Fukuchi, K., Tomoyasu, S., Tsuruoka, N., and Gomi, K., Iron deprivation-induced apoptosis in HL-60 cells. FEBS Lett., 350, 139-142 (1994).
  • 20) Frenandez-Pol, J. A., Bono, V. H., and Johnson, G. E., Control of growth by picolinic acid: differential response of normal and transformed cells. Proc. Natl. Acad. Sci. USA, 74, 2889-2893 (1977).
  • 21) Lynn, D. G., Nakanishi, K., Patt, S. L., Occolowitz, J. L., Almeida, S., and Evans, L. S., Isolation and characterization of first mitotic cycle hormone that regulates cell proliferation. J. Am. Chem. Soc., 100, 7759-7760 (1978).
  • 22) Ueda, K. and Banasik, M., Inhibitors and activators of ADP-ribosylation reactions. Mol. Cell. Biochem., 138, 185-197 (1994).
  • 23) Perkins, M. N., and Stone, T. W., An iontophoretic investigation of the actions of convulsant kynurenines and their interaction with the endogenous excitant quinolinic acid. Brain Res., 247, 184-187 (1982).
  • 24) Kawashima, T., Sanaka, T., Sugino, N., Takahashi, M., and Mizoguchi, H., Suppressive effect of quinolinic acid and hippuric acid on bone marrow erythroid growth and lymphocyte blast formation in uremia. Adv. Exp. Med. Biol., 223, 69-72 (1987).
  • 25) Hoshino, J., Kühne, U., and Kröger, H., Enhancement of DNA synthesis and cell proliferation by 1-methylnicotinamide in rat liver cells in culture. Biochem. Biophys. Res. Commun., 105, 1446-1452 (1982).
  • 26) Enari, M., Talanian, R. V., Wong, W. W., and Nagata, S., Sequential activation of ICE-like and CPP32-like proteases during Fas-mediated apoptosis. Nature, 380, 723-726 (1996).
  • 27) Boldin, M. P., Goncharov, T. M., Goltsev, Y. V., and Wallach, D., Involvement of MACH, a novel MORT1/FADD-interacting protease, in Fas/APO-1- and TNF receptor-induced cell death. Cell, 85, 803-815 (1996).
  • 28) Muzio, M., Chinnaiyan, A. M., Kischkel, F. C., O’Rourke, K., Shevchenko, A., Ni, J., Scaffidi, C., Bretz, J. D., Zhang, M., Gentz, R., Mann, M., Krammer, P. H., Peter, M. E., and Dixit, V. M., FLICE, a novel FADD-homologous ICE/CED-3-like protease, is recruited to the CD95 (Fas/APO-1) death-inducing signaling complex. Cell, 85, 817-827 (1996).
  • 29) Faleiro, L., Kobayashi, R., Fearnhead, H., and Lazebnik, Y., Multiple species of CPP32 and Mch2 are the major active caspases present in apoptotic cells. EMBO J., 16, 2271-2281 (1997).
  • 30) Polverino, A. J., and Patterson, S. D., Selective activation of caspases during apoptotic induction in HL-60 cells. Effects of a tetrapeptide inhibitor. J. Biol. Chem., 272, 7013-7021 (1997).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.