| Title |
Cancer cell-derived IL-8 induces monocytic THP1 cells to secrete IL-8 via the mitogen-activated protein kinase pathway
|
|---|---|
| Published in |
Tumor Biology, June 2015
|
| DOI | 10.1007/s13277-015-3641-6 |
| Pubmed ID | |
| Authors |
Yukina Nishio, Takahiro Gojoubori, Yasuhide Kaneko, Noriyoshi Shimizu, Masatake Asano |
| Abstract |
Aberrant activity of transcription factors in oral squamous cell carcinoma (OSCC) results in the spontaneous secretion of various cytokines and chemokines. Among them, IL-8, owing to its angiogenic activity, promotes the growth of OSCCs. In the present study, we examined the role of IL-8 secreted by OSCCs, on the angiogenic activity of monocytic THP1 cells. Culture supernatant (Ca-sup) augmented IL-8 secretion by THP1 cells, which was found to be significantly reduced following the removal Ca9-22-derived IL-8 from the Ca-sup. IL-8 induction was regulated at the transcriptional level, because real-time PCR demonstrated the augmented IL-8 messenger RNA (mRNA) expression. We further performed the luciferase assay using the 5'-untranslated region of IL-8 gene. Contradictory to our speculations, luciferase activity was not augmented by Ca-sup stimulation. NF-κB-independent IL-8 induction was further confirmed by pre-treating THP1 cells with NF-κB-specific inhibitors. To elucidate the signaling pathway, THP1 was pre-treated with MEK inhibitors. The results demonstrated that pre-treatment of cells with MEK inhibitor drastically reduced IL-8 levels, suggesting the role of MEK. Moreover, Ca-sup was found to increase ERK1/2 phosphorylation in a time-dependent manner. These results indicated that OSCC-derived IL-8 appears to activate angiogenic activity in monocytes within the tumor microenvironment via the mitogen-activated protein kinase (MAPK) pathway. |
X Demographics
The data shown below were collected from the profile of 1 X user who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 1 | 100% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 1 | 100% |
Mendeley readers
The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 20 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Bachelor | 3 | 15% |
| Student > Doctoral Student | 2 | 10% |
| Researcher | 2 | 10% |
| Student > Master | 2 | 10% |
| Professor | 1 | 5% |
| Other | 2 | 10% |
| Unknown | 8 | 40% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 6 | 30% |
| Biochemistry, Genetics and Molecular Biology | 3 | 15% |
| Chemical Engineering | 1 | 5% |
| Immunology and Microbiology | 1 | 5% |
| Materials Science | 1 | 5% |
| Other | 0 | 0% |
| Unknown | 8 | 40% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 14 August 2015.
All research outputs
#18,422,065
of 22,821,814 outputs
Outputs from Tumor Biology
#1,369
of 2,622 outputs
Outputs of similar age
#190,051
of 264,720 outputs
Outputs of similar age from Tumor Biology
#66
of 158 outputs
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