Porphyromonas gingivalis promotes invasion of oral squamous cell carcinoma through induction of proMMP9 and its activation
Version of Record online: 19 SEP 2013
© 2013 John Wiley & Sons Ltd
Volume 16, Issue 1, pages 131–145, January 2014
How to Cite
Inaba, H., Sugita, H., Kuboniwa, M., Iwai, S., Hamada, M., Noda, T., Morisaki, I., Lamont, R. J. and Amano, A. (2014), Porphyromonas gingivalis promotes invasion of oral squamous cell carcinoma through induction of proMMP9 and its activation. Cellular Microbiology, 16: 131–145. doi: 10.1111/cmi.12211
- Issue online: 13 DEC 2013
- Version of Record online: 19 SEP 2013
- Accepted manuscript online: 2 SEP 2013 05:00AM EST
- Manuscript Accepted: 15 AUG 2013
- Manuscript Revised: 2 AUG 2013
- Manuscript Received: 5 JUN 2013
- Ministry of Education, Culture, Sports, Science and Technology of Japan. Grant Numbers: 23792102, 25462850, B23390477
- NIH. Grant Numbers: DE11111, DE17921
Supporting Experimental Procedures.
Fig. S1. Effects of SAS cell supernatant after infection with P. gingivalis on cell invasion of Ca9-22 cells. We determined Ca9-22 cell invasion through matrigel-coated transwell membranes at 24 h with and without the supernatant of SAS cells infected with P. gingivalis at an moi of 1. Data are shown as the mean ± SD of three independent experiments.*P < 0.01 (t-test).
Fig. S2. Effects of NF-kB inhibitor, p38, JNK and ERK1/2-specific inhibitors on cell morphology and proliferation of SAS cells.
A. Light microscopy images showing morphology of SAS cells treated with the inhibitors for 24 h. Control cells were untreated.
B. The proliferation of SAS cells was determined using tetrazolium following treatment with/without the inhibitors for 24 h. Data are expressed as relative to the ratio of treated/untreated (c) and shown as the mean ± SD of three independent experiments. The results were analysed with a t-test.
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