500
Views
4
CrossRef citations to date
0
Altmetric
Research Article

Inhibition of NF-κB signaling interferes with phorbol ester-induced growth arrest of keratinocytes in a TNFR1-independent manner

, , &
Pages 44-51 | Received 02 Oct 2008, Accepted 10 Dec 2008, Published online: 01 Feb 2009

References

  • Karin M. Nuclear factor-kappaB in cancer development and progression. Nature (2006), 441(7092), 431–436.
  • Krammer PH, Arnold R, Lavrik IN. Life and death in peripheral T cells. Nat Rev Immunol (2007), 7(7), 532–542.
  • Seitz CS, Deng H, Hinata K, Lin Q, Khavari PA. Nuclear factor kappaB subunits induce epithelial cell growth arrest. Cancer Res (2000), 60(15), 4085–4092.
  • van Hogerlinden M, Rozell BL, Ahrlund-Richter L, Toftgard R. Squamous cell carcinomas and increased apoptosis in skin with inhibited Rel/nuclear factor-kappaB signaling. Cancer Res (1999), 59(14), 3299–3303.
  • Pasparakis M, Courtois G, Hafner M, et al. TNF-mediated inflammatory skin disease in mice with epidermis-specific deletion of IKK2. Nature (2002), 417(6891), 861–866.
  • Lind MH, Rozell B, Wallin RP, et al. Tumor necrosis factor receptor 1-mediated signaling is required for skin cancer development induced by NF-kappaB inhibition. Proc Natl Acad Sci U S A (2004),101(14), 4972–4977.
  • Dajee M, Lazarov M, Zhang JY, et al. NF-kappaB blockade and oncogenic Ras trigger invasive human epidermal neoplasia. Nature (2003), 421(6923), 639–643.
  • Zhang JY, Adams AE, Ridky TW, Tao S, Khavari PA. Tumor necrosis factor receptor 1/c-Jun-NH2-kinase signaling promotes human neoplasia. Cancer Res (2007), 67(8), 3827–3834.
  • Zhang JY, Tao S, Kimmel R, Khavari PA. CDK4 regulation by TNFR1 and JNK is required for NF-kappaB-mediated epidermal growth control. J Cell Biol (2005), 168(4), 561–566.
  • Zhang JY, Green CL, Tao S, Khavari PA. NF-kappaB RelA opposes epidermal proliferation driven by TNFR1 and JNK. Genes Dev (2004), 18(1), 17–22.
  • van Hogerlinden M, Auer G, Toftgard R. Inhibition of Rel/Nuclear Factor-kappaB signaling in skin results in defective DNA damage-induced cell cycle arrest and Ha-ras- and p53-independent tumor development. Oncogene (2002), 21(32), 4969–4977.
  • Campbell C, Quinn AG, Rees JL. Codon 12 Harvey-ras mutations are rare events in non-melanoma human skin cancer. Br J Dermatol (1993), 128(2), 111–114.
  • Rumsby G, Carter RL, Gusterson BA. Low incidence of ras oncogene activation in human squamous cell carcinomas. Br J Cancer (1990), 61(3), 365–368.
  • Dickson MA, Hahn WC, Ino Y, et al. Human keratinocytes that express hTERT and also bypass a p16(INK4a)-enforced mechanism that limits life span become immortal yet retain normal growth and differentiation characteristics. Mol Cell Biol (2000), 20(4), 1436–1447.
  • Denning MF. Epidermal keratinocytes: Regulation of multiple cell phenotypes by multiple protein kinase C isoforms. Int J Biochem Cell Biol (2004), 36(7), 1141–1146.
  • Brose N, Rosenmund C. Move over protein kinase C, you’ve got company: alternative cellular effectors of diacylglycerol and phorbol esters. J Cell Sci (2002), 115(Pt 23), 4399–4411.
  • Moore RJ, Owens DM, Stamp G, et al. Mice deficient in tumor necrosis factor-alpha are resistant to skin carcinogenesis. Nat Med (1999), 5(7), 828–831.
  • Suganuma M, Okabe S, Marino MW, Sakai A, Sueoka E, Fujiki H. Essential role of tumor necrosis factor alpha (TNF-alpha) in tumor promotion as revealed by TNF-alpha-deficient mice. Cancer Res (1999), 59(18), 4516–4518.

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.