IL-37 promotes cell apoptosis in cervical cancer involving Bim upregulation.
Onco Targets Ther
; 12: 2703-2712, 2019.
Article
em En
| MEDLINE
| ID: mdl-31114224
ABSTRACT
Background:
Growing evidence has indicated that interleukin-37 (IL-37) is a potential anticancer molecule that mainly plays an inhibiting role in different kinds of cancers, but data for the role of IL-37 on cell apoptosis in cancers remains rare. The present study aimed to explore the role of IL-37 in cell apoptosis in cervical cancer, and the involved apoptosis-related molecules.Methods:
IL-37 was overexpressed by transfecting the pIRES2-EGFP-IL-37 plasmid in HeLa and C33A cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was performed to detect the mRNA expression of IL-37, Bcl-2, Bax and Bim. Western blotting was performed to detect the protein expression of IL-37 and Bim. Cell apoptosis was detected by flow cytometry.Results:
IL-37 upregulated the mRNA expression levels of Bim by 138.40% for HeLa (P<0.05) and 58.95% for C33A (P<0.05), and increased the protein expression levels of BimL by 69.10% (P<0.05) and 56.66% (P<0.05) in HeLa and C33A, respectively. Overexpression of IL-37 increased the apoptosis rates by 152.86% for HeLa (P<0.01) and 25.4% for C33A (P<0.05). Knockdown of Bim by specific siRNA interference fragments (SiBim) reduced the apoptosis rates by 36.00% for HeLa (P<0.05) and 14.66% for C33A (P<0.05). Compared with the IL-37 overexpression group, the apoptosis rate in cotransfecting the IL-37 overexpression plasmid and SiBim group decreased by approximately 31% (P<0.05) and 24.35% (P<0.05) in HeLa and C33A, respectively.Conclusion:
IL-37 upregulated Bim in cervical cancer cells. Furthermore, IL-37 can promote cervical cancer cell apoptosis, but Bim knockdown decreased this promotion through IL-37. Thus, IL-37 can promote cervical cancer cell apoptosis, which involve the upregulation of Bim.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Revista:
Onco Targets Ther
Ano de publicação:
2019
Tipo de documento:
Article