PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

IL-36α suppresses proliferation of ovarian cancer cells.

Abstract Interleukin-36α (IL-36α), also formerly known as IL-1F6, is pertaining to IL-1 family members that has been shown to play an important pro-inflammatory role in chronic immune disorders. However, the role IL-36α in the setting of cancer remains unknown. Here, in our study, to investigate the clinical relevance of IL-36α in ovarian cancer, clinicopathological significance as well as expression level of IL-36α were analyzed in epithelial ovarian cancer clinical tissues and paired normal control. To explore the biological role of IL-36α in vitro in epithelial ovarian cancer cells, both overexpression and knockdown of IL-36α were performed. Based on the successful re-expression and silencing of IL-36α, proliferation, migration, and invasion were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, wound-healing, and Transwell assays, respectively. To further confirm the effect over proliferation in vivo, nude mice xenografted with epithelial ovarian cancer cells whose endogenous IL-36α was stably upregulated or downregulated were employed. It was found that IL-36α was shown to be markedly downregulated in epithelial ovarian cancer tissues relative to paired normal control and that reduced IL-36α expression was significantly associated with poor overall prognosis. In addition, IL-36α was observed to be able to suppress the growth of epithelial ovarian cancer cells both in vivo and in vitro. Taken together, IL-36α was displayed to be able to suppress the growth of epithelial ovarian cancer cells in our setting, which is suggestive of its druggable potential in curing the epithelial ovarian cancer and that upregulation of IL-36α was found to be capable of inhibiting the growth of epithelial ovarian cancer cells.
PMID
Related Publications

Downregulation of matrix metalloproteinase 9 by small interfering RNA inhibits the tumor growth of ovarian epithelial carcinoma in vitro and in vivo.

NFATc1 regulates cell proliferation, migration, and invasion of ovarian cancer SKOV3 cells in vitro and in vivo.

Decreased expression of interleukin-36α correlates with poor prognosis in hepatocellular carcinoma.

Downregulation of glypican-3 expression increases migration, invasion, and tumorigenicity of human ovarian cancer cells.

The role of Sox6 and Netrin-1 in ovarian cancer cell growth, invasiveness, and angiogenesis.

Authors

Mayor MeshTerms

Prognosis

Keywords

Ovarian cancer

interleukin-36α

migration

prognosis

proliferation

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28621240
OWN - NLM
STAT- MEDLINE
DA  - 20170616
DCOM- 20170622
LR  - 20170622
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - IL-36alpha suppresses proliferation of ovarian cancer cells.
PG  - 1010428317706918
LID - 10.1177/1010428317706918 [doi]
AB  - Interleukin-36alpha (IL-36alpha), also formerly known as IL-1F6, is pertaining to
      IL-1 family members that has been shown to play an important pro-inflammatory
      role in chronic immune disorders. However, the role IL-36alpha in the setting of 
      cancer remains unknown. Here, in our study, to investigate the clinical relevance
      of IL-36alpha in ovarian cancer, clinicopathological significance as well as
      expression level of IL-36alpha were analyzed in epithelial ovarian cancer
      clinical tissues and paired normal control. To explore the biological role of
      IL-36alpha in vitro in epithelial ovarian cancer cells, both overexpression and
      knockdown of IL-36alpha were performed. Based on the successful re-expression and
      silencing of IL-36alpha, proliferation, migration, and invasion were evaluated
      using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide,
      wound-healing, and Transwell assays, respectively. To further confirm the effect 
      over proliferation in vivo, nude mice xenografted with epithelial ovarian cancer 
      cells whose endogenous IL-36alpha was stably upregulated or downregulated were
      employed. It was found that IL-36alpha was shown to be markedly downregulated in 
      epithelial ovarian cancer tissues relative to paired normal control and that
      reduced IL-36alpha expression was significantly associated with poor overall
      prognosis. In addition, IL-36alpha was observed to be able to suppress the growth
      of epithelial ovarian cancer cells both in vivo and in vitro. Taken together,
      IL-36alpha was displayed to be able to suppress the growth of epithelial ovarian 
      cancer cells in our setting, which is suggestive of its druggable potential in
      curing the epithelial ovarian cancer and that upregulation of IL-36alpha was
      found to be capable of inhibiting the growth of epithelial ovarian cancer cells.
FAU - Chang, Lei
AU  - Chang L
AD  - Department of Gynecology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, P.R. China.
FAU - Guo, Ruixia
AU  - Guo R
AD  - Department of Gynecology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, P.R. China.
FAU - Yuan, Zhongfu
AU  - Yuan Z
AD  - Department of Gynecology, The First Affiliated Hospital of Zhengzhou University, 
      Zhengzhou, P.R. China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (IL36A protein, human)
RN  - 0 (Interleukin-1)
SB  - IM
MH  - Animals
MH  - Cell Movement/genetics
MH  - Cell Proliferation/*genetics
MH  - Disease-Free Survival
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Interleukin-1/biosynthesis/*genetics
MH  - Mice
MH  - Neoplasm Invasiveness/genetics
MH  - Neoplasm Staging
MH  - Ovarian Neoplasms/*genetics/pathology
MH  - *Prognosis
MH  - Xenograft Model Antitumor Assays
OTO - NOTNLM
OT  - Ovarian cancer
OT  - interleukin-36alpha
OT  - migration
OT  - prognosis
OT  - proliferation
EDAT- 2017/06/18 06:00
MHDA- 2017/06/24 06:00
CRDT- 2017/06/17 06:00
AID - 10.1177/1010428317706918 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317706918. doi: 10.1177/1010428317706918.