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Association between interleukin‑33 and ovarian cancer
Xiaoqing Liu1, Dwayne M Hansen2, Noah J Timko3
1Department of Anatomy, Anhui College of Traditional Chinese Medicine, Wuhu, Anhui 241000, P.R. China.
Oncology Reports
|December 12, 2018
Summary
Interleukin-33 (IL-33) promotes ovarian cancer cell proliferation and survival by downregulating key proteins. This finding suggests IL-33 inhibition as a potential therapeutic strategy for ovarian cancer.
Area of Science:
- Oncology
- Immunology
- Molecular Biology
Background:
- Ovarian cancer is a leading cause of reproductive system cancer mortality.
- Interleukin-33 (IL-33) and its receptor ST2 are expressed in epithelial cells, with a controversial role in neoplasia.
- Previous studies showed IL-33 inhibits pancreatic cancer growth.
Purpose of the Study:
- To investigate the direct effects of IL-33 on ovarian cancer cell proliferation and apoptosis.
- To explore the molecular mechanisms underlying IL-33's action in ovarian cancer.
Main Methods:
- Utilized A2780 ovarian cancer cell line.
- Employed clonogenic survival assay, immunohistochemistry (IHC), proliferation kit, and caspase-3 activity assay.
- Performed reverse transcription-polymerase chain reaction (RT-PCR) and IHC for molecular analysis.
Main Results:
- IL-33 increased ovarian cancer cell colony formation and proliferation.
- IL-33 decreased caspase-3 activity, indicating reduced apoptosis.
- IL-33's pro-proliferative effect correlated with decreased p27 levels.
- IL-33's anti-apoptotic effect correlated with levels of Fas and TRAILR1.
Conclusions:
- IL-33 promotes ovarian cancer cell proliferation and inhibits apoptosis.
- This effect is mediated by the downregulation of p27, Fas, and TRAILR1.
- IL-33 exhibits an onco-promoting role in ovarian cancer, unlike its effect in pancreatic cancer.
- Inhibiting IL-33 may represent a promising therapeutic strategy for ovarian cancer.
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