Journal
JOURNAL OF CANCER
Volume 6, Issue 10, Pages 962-969Publisher
IVYSPRING INT PUBL
DOI: 10.7150/jca.12266
Keywords
Interleukin 37; Cervical cancer; Proliferation; Invasion
Categories
Funding
- National Natural Science Foundation of China [81302244]
- Industrial technology research and development special fund project of Guangdong Province [2013B021800062]
- Social Science and Technology Development Project of Dongguan [2013108101051, 201410515200188]
- Natural Science Foundation of Guangdong Province [S2012040006383]
- Medical Science and Technology Research Fund of Guangdong province [B2013293]
- PhD Start-up Fund of Guangdong Medical College [B2011012, B2011015, B2011019]
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Objectives: The most recently discovered cytokine interleukin 37 (IL-37) received growing attention. Its function on tumor is largely unknown. Here, we investigated the biological function of IL-37 on cervical cancer (CC). Materials and methods: HPV+ Hela cells and HPV- C33A cells were used. RT-qPCR was performed to detect the transcription of IL-37, STAT3, TNF-alpha and IL-1 beta. Western blotting was used for protein detection. CCK-8 assay and transwell assay were employed for cell proliferation and invasion detection, respectively. Results: Successful gene transfection of IL-37 suppressed the proliferation and invasion of CC. Interestingly, IL-37 showed higher anticancer ability in HPV+ Hela cells than that in HPV- C33A cells. Then, the molecular mechanism of IL-37 anticancer was explored. Firstly, we found that IL-37 inhibited STAT3 expression at both mRNA and protein levels. IL-37 also down regulated the phosphorylation of STAT3. Secondly, blockage of STAT3 using siRNAs reduced significantly the ability of IL-37 to suppress cell proliferation and invasion. Thirdly, STAT3 knockdown reduced markedly the inhibition of IL-37 on the transcription of tumor-derived TNF-alpha and IL-1 beta, indicating the contribution of STAT3 for the cancer associated antiinflammation of IL-37. Finally, STAT3 up regulation restored the ability of cell proliferation, cell invasion and the expression of inflammatory cytokines, TNF-alpha and IL-1 beta. Conclusions: IL-37 suppressed cell proliferation and invasion of CC and STAT3 is involved in this process. Thus, IL-37 emerges as a new anticancer cytokine for CC. This study demonstrated a new biological function of IL-37 and offered a potential molecule for CC treatment.
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