39P - IL-6 induces and releasing of MMP-9 in murine bone marrow neutrophils by activating STAT3 pathway

Date 10 October 2016
Event ESMO 2016 Congress
Session Poster display
Topics Basic Science
Presenter xufeng Wu
Citation Annals of Oncology (2016) 27 (6): 1-14. 10.1093/annonc/mdw362
Authors X. Wu1, B. Yan2
  • 1Gynecological Oncology, Hubei Maternity and Child Health Hospital, 430070 - Wuhan/CN
  • 2Gynecological Oncology, Hubei Maternity and Child health hospital, 430070 - Wuhan/CN

Abstract

Background

To investigate the production and release of murine bone marrow neutrophil MMP-9 and its mechanism of activation.

Methods

Murine bone marrow neutrophils were separated and cultured in vitro and randomly divided into four groups: control group, IL-6 50ng/ml stimulation group, IL-6 50ng/ml + DMSO group and IL-6 50ng/ml + STAT3 inhibitor VIII 50 µM group. RT-PCR method was used to evaluate the mRNA level of intracellular MMP-9 of neutrophils. Gelatin zymography was performed to detect the activity of MMP-9 released from neutrophils. Western blot was applied to test the phosphorylation levels of STAT3 pathway in neutrophils.

Results

Compared with the control group, the administration of IL-6 enhanced the mRNA expression of MMP-9 (P = 0.0050); the activity of MMP-9 released from neutrophils was elevated (P = 0.0087) and the p-STAT3 levels in neutrophils was also increased (P =0.089). After the STAT3 inhibitor VIII was added, the mRNA expression of MMP-9, the activities of MMP-9 in the supernatant and the p-STAT3 levels in neutrophils were decreased significantly compared with those in the IL-6 group (P = 0.0067, 0.048 and 0.098, respectively).

Conclusions

IL-6 induces the production and releasing of MMP-9 in neutrophils and the effect may be induced by the activation of STAT3 pathway.

Clinical trial identification

Legal entity responsible for the study

Hubei Maternity and Child Health Hospital

Funding

Hubei Maternity and Child Health Hospital

Disclosure

All authors have declared no conflicts of interest.