British Journal of Cancer (2000) 82, 28–33. doi:10.1054/bjoc.1999.0872 www.bjcancer.com
Published online 10 December 1999
Inhibition of I
B-
phosphorylation at serine and tyrosine acts independently on sensitization to DNA damaging agents in human glioma cells
J Miyakoshi1 and K Yagi2
- 1Department of Radiation Genetics, Graduate School of Medicine Yoshida-Konoe-cho, Sakyo-ku, 606-8501, Japan
- 2Department of Zoology, Graduate School of Science, Kyoto University, Yoshida-Konoe-cho, Sakyo-ku, 606-8501, Japan
Received 14 January 1999; Revised 17 June 1999; Accepted 21 June 1999.
Top of pageAbstract
Molecular mechanisms and/or intrinsic factors controlling cellular radiosensitivity are not fully understood in mammalian cells. The recent studies have suggested that nuclear factor
B (NF-
B) is one of such factors. The activation and regulation of NF-
B are tightly controlled by I
B-
, a cellular inhibitory protein of NF-
B. Most importantly, phosphorylation regulates activity of the inhibitor I
B-
, which sequesters NF-
B in the cytosol. Two different pathways for the phosphorylation of I
B-
are demonstrated, such as serine (at residues 32 and 36) and tyrosine (at residue 42) phosphorylations. To assess a role of the transcription factor, NF-
B, on cellular sensitivity to DNA damaging agents, we constructed three different types of expression plasmids, i.e. S-I
B (mutations at residues 32 and 36), Y-I
B (mutation at residue 42) and SY-I
B (mutations at residues 32, 36 and 42). The cell clones expressing S-I
B and Y-I
B proteins became sensitive to X-rays as compared with the parental and vector-transfected cells. The cell clones expressing SY-I
B were further radiosensitive. By the treatment with herbimycin A, an inhibitor of phosphorylation, the X-ray sensitivity of cells expressing SY-I
B did not change, while that of the cells expressing S-I
B and Y-I
B and the parental cells was enhanced. Change in the sensitivity to adriamycin and UV in those clones was very similar to that in the X-ray sensitivity. The inhibition of I
B-
phosphorylation at serine and tyrosine acts independently on the sensitization to X-rays, adriamycin and UV. These findings suggest that the transcriptional activation induced by NF-
B may play a role in the DNA damage repair. The present study proposes a possibility that the inactivation of NF-
B by inhibition of both serine and tyrosine phosphorylations may be useful for the treatment of cancer in radio- and chemotherapies. © 2000 Cancer Research Campaign
Top of pageReferences
- Alkalay I, Yaron A, Hatzubai A, Orian A, Ciechanover A and Ben-Neriah Y (1995) Stimulation-dependent I
B
phosphorylation marks the NF-
B inhibitor for degradation via the ubiquitin-proteasome pathway. Proc Natl Acad Sci USA 92: 10599–10603 | Article | PubMed | ChemPort | - Baeuerle PA (1991) The inducible transcription activator NF-
B: regulation by distinct protein subunits. Biochim Biophys Acta 1072: 63–80 | Article | PubMed | ISI | ChemPort | - Baeuerle PA and Baltimore D (1988) I
B-
: a specific inhibitor of the NF-
B transcription factor. Science 242: 540–546 | Article | PubMed | ISI | ChemPort | - Baeuerle PA and Henkel T (1994) Function and activation of NF-
B in immune system. Annu Rev Immunol 12: 141–179 | Article | PubMed | ISI | ChemPort | - Beg AA, Rubin SM, Scheinman RI, Haskill S, Rosen CA and Baldwin AS (1992) I
B interacts with the nuclear locatization sequencers of the subunits of NF-
B: a mechanism for cytoplasmic retention. Genes Dev 6: 1899–1913 | Article | PubMed | ISI | ChemPort | - Beg AA, Finc TS, Nantermet PV and Baldwin AS Jr (1993) Tumor necrosis factor and interleukin-1 lead to phosphorylation and loss of I
B-
: a mechanism for NF-
B activation. Mol Cell Biol 13: 13301–13310 - Brockman JA, Scherer DC, McKinsey TA, Hall SM, Qi X, Young Lee W and Ballard DW (1995) Coupling of a signal response domain in I
B
to multiple pathways for NF-
B activation. Mol Cell Biol 15: 2809–2818 | PubMed | ISI | ChemPort | - Brown K, Park S, Kanno T, Franzoso G and Siebenlist U (1993) Mutual regulation of the transcriptional activator NF-
B and its inhibitor, I kappa B-
. Proc Natl Acad Sci USA 90: 2532–2536 | Article | PubMed | ChemPort | - Brown K, Gerstberger S, Carlson L, Franzoso G and Siebenlist U (1995) Control of I
B-
proteolysis by site-specific, signal-induced phosphorylation. Science 267: 1485–1488 | Article | PubMed | ISI | ChemPort | - Cordle SR, Donald R, Read MA and Hawiger J (1993) Lipopolysaccharide induces phosphorylation of MAD3 and activation of c-Rel and related NF-
B proteins in human monocytic THP-1 cells. J Biol Chem 268: 11803–11810 | PubMed | ISI | ChemPort | - Hallahan DE, Sukhatme VP, Sherman ML, Virudaghalam S, Kufe D and Weichselbaum RR (1991) Protein kinase C mediates x-ray inducibility of nuclear signal transducers EGR1 and JUN. Proc Natl Acad Sci USA 88: 2156–2160 | Article | PubMed | ChemPort |
- Imbert V, Rupec RA, Livolsi A, Pah HL, Traenckner EB-M, Mueller-Dieckman C, Farahifer D, Rossi B, Auberger P, Baeuerle PA and Peyron J-F (1996) Tyrosine phosphorylation of I
B-
activates NF-
B without proteolytic degradation of I
B-
. Cell 86: 787–798 | Article | PubMed | ISI | ChemPort | - Iwasaki T, Uehara Y, Gravea L, Rachie N and Bomsztyk K (1992) Herbimycin A blocks IL-1-induced NF-
B DNA-binding activity in lymphoid cell lines. FEBS Lett 298: 240–244 | PubMed | - Jung M, Zhang Y, Lee S and Dritschilo A (1995) Correction of radiation sensitivity in Ataxia Telangiectasia cells by a truncated I
B-
. Science 268: 1619–1621 | PubMed | ISI | ChemPort | - Kasid U, Pfeifer A, Brenman T, Beckett M, Weichselbaum RR, Dritschilo A and Mark GE (1989) Effect of antisense c- raf -1 on tumorigenicity and radiation sensitivity of a human squamous carcinoma. Science 243: 1354–1356 | PubMed | ISI | ChemPort |
- Mellits KH, Hay RT and Goodbourn S (1993) Proteolytic degradation of MAD3 (I
B alpha) and enhanced processing of the NF-
B precursor p105 are obligatory steps in the activation of NF-
B. Nucelic Acids Res 21: 5059–5066 - Miyakoshi J, Yamagishi N, Ohtsu S and Takebe H (1995) Changes in radiation sensitivity of human osteosarcoma cells after p53 introduction. Jap J Cancer Res 86: 711–713
- Miyakoshi J, Yamagishi N, Ohtsu S, Mohri K and Takebe H (1996) Exposure to magnetic field (5 mT at 60 Hz) does not affect cell growth and c-myc gene expression. Mutat Res 349: 109–114
- Miyakoshi J, Kitagawa K, Yamagishi N, Ohtsu S, Day RSIII and Takebe H (1997) Increased radiosensitivity of p16 gene-deleted human glioma cells after transfection with wild-type p16 gene. Jap J Cancer Res 88: 34–38
- Morhan N and Meltz ML (1994) Induction of nuclear factor
B after low-dose ionizing radiation involves a reactive oxygen intermediate signaling pathway. Radiat Res 140: 97–104 | PubMed | ISI | ChemPort | - Pirollo KF, Tong YA, Villegas Z, Chen Y and Chang EH (1993) Oncogene-transformed NIH 3T3 cells display radiation resistance levels indicative of a signal transduction pathway leading to the radiation-resistant phenotype. Radiat Res 135: 234–243 | PubMed |
- Scherer DC, Brockman JA, Chen Z, Maniatis T and Ballard DW (1995) Signal-induced degradation of I
B
requires site-specific ubiquitination. Proc Natl Acad Sci USA 92: 11259–11263 | Article | PubMed | ChemPort | - Schreiber E, Matthias P, Mulle MM and Schaffner W (1989) Rapid detection of octamer binding proteins with 'mini-extracts', prepared from a small number of cells. Nucleic Acids Res 17: 6419 | Article | PubMed | ISI | ChemPort |
- Sklar MD (1988) The ras oncogenes increase the intrinsic resistance of HIH 3T3 cells to ionizing radiation. Science 239: 645–647 | Article | PubMed | ISI | ChemPort |
- Traenckner EB-, Pahl HL, Henke T, Schmidt KN, Wilk S and Baererle PA (1995) Phosphorylation of human I
B-
on serines 32 and 36 control I
B-
proteolysis and NF-
B activation in response to diverse stimuli. EMBO J 14: 2876–2883 | PubMed | ISI | ChemPort | - Uckun FM, Schieven GL, Tuel-Ahlgren LM, Dibirdik I, Myers DE, Ledbetter JA and Song CW (1993) Tyrosine phosphorylation is a mandatory proximal step in radiation-induced activation of the protein kinase C signaling pathway in human B-lymphocyte precursors. Proc Natl Acad Sci USA 90: 252–256 | Article | PubMed | ChemPort |
- Yamagishi N, Miyakoshi J and Takebe H (1997 a) Decrease in the frequency of x-ray-induced mutation by wild-type p53 protein in human osteosarcoma cells. Carcinogenesis 18: 695–700
- Yamagishi N, Miyakoshi J, Yagi T and Takebe H (1997 b) Suppression of UV-induced mutation by wild-type p53 protein in human osteosarcoma cells. Mutagenesis 12: 191–194
- Verma IM, Stevenson JK, Schwarz EM, Van Antwerp D and Miyamoto S (1995) Rel/NF-
B family: intimate tales of association and dissociation. Genes Dev 9: 2723–2735 | Article | PubMed | ISI | ChemPort | - Wang C-Y, Mayo MW and Baldwin AS Jr (1996) TNF- and cancer therapy-induced apoptosis: potentiation by inhibition of NF-
B. Science 274: 784–787 | Article | PubMed | ISI | ChemPort | - Wilson RE, Taylor SL, Atherton GT, Johnston D, Waters CM and Norton JD (1993) Early response gene signalling cascades activated by ionizing radiation in primary human B cells. Oncogene 8: 3229–3237 | PubMed |