JunB can enhance the transcription of IL-8 in oral squamous cell carcinoma.
Carcinoma, Squamous Cell
/ genetics
Cell Line, Tumor
Humans
Interleukin-8
/ genetics
Mouth Neoplasms
/ genetics
Promoter Regions, Genetic
/ genetics
Proto-Oncogene Proteins c-fos
/ genetics
Proto-Oncogene Proteins c-jun
/ genetics
RNA, Messenger
/ genetics
Transcription Factors
/ genetics
Transcription, Genetic
/ genetics
Transcriptional Activation
/ genetics
Transfection
/ methods
IL-8 oral squamous cell carcinoma
JunB
MG132
c-Jun
Journal
Journal of cellular physiology
ISSN: 1097-4652
Titre abrégé: J Cell Physiol
Pays: United States
ID NLM: 0050222
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
09
02
2020
revised:
25
05
2020
accepted:
25
05
2020
pubmed:
9
6
2020
medline:
28
8
2021
entrez:
9
6
2020
Statut:
ppublish
Résumé
Proteasome inhibitor MG132 was shown to enhance the secretion of interleukin 8 (IL-8) by various cells. The enhancement is regulated by the transcription factor activator protein-1 (AP-1) at the transcriptional level. AP-1 is a dimer formed by AP-1 family proteins. The purpose of the present study was to explore the combinations of the AP-1 family proteins that contribute to MG132-driven IL-8 secretion. Oral squamous cell carcinoma-derived cell lines, Ca9-22 and HSC3, were used to demonstrate their response to MG132. IL-8 secretion was augmented by MG132 in both cell lines. c-Jun expression was detected in both the cell lines, whereas c-Fos expression was detected only in the HSC3. The influence of MG132 stimulation on c-Jun and c-Fos expression was further examined by western blot analysis. c-Jun expression was increased by MG132 stimulation, whereas c-Fos expression was not detected even after MG132 stimulation. As JunB is reported to inhibit the transcriptional activity of the AP-1 complex, we speculated that the c-Jun homodimer should contribute to IL-8 enhancement. Expression vectors encoding wild type and c-Jun mutants, M17 and M22-23, respectively, were constructed and transfected into the Ca9-22 cells. In contrast to our expectations, MG132-induced IL-8 secretion was significantly reduced in all the transfectants suggesting that other c-Jun members might form homodimers with c-Jun and contribute to IL-8 enhancement. Transfection of the cells with c-Jun or JunB small hairpin RNA (shRNA) reduced IL-8 secretion up to 50% and 65% of the control shRNA transfectant. Furthermore, cotransfection of both shRNA almost completely inhibited the IL-8 secretion. These results indicate that JunB not only inhibits but also enhances the transcription of c-Jun targets in combination with c-Jun.
Substances chimiques
Interleukin-8
0
JunB protein, human
0
Proto-Oncogene Proteins c-fos
0
Proto-Oncogene Proteins c-jun
0
RNA, Messenger
0
Transcription Factors
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
309-317Informations de copyright
© 2020 Wiley Periodicals LLC.
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