Effects of Oxytocin on Cell Proliferation in a Corticotroph Adenoma Cell Line
Endocrinology and Metabolism
; : 302-313, 2019.
Article
in En
| WPRIM
| ID: wpr-763710
Responsible library:
WPRO
ABSTRACT
BACKGROUND:
Oxytocin (OXT) has been reported to act as a growth regulator in various tumor cells. However, there is a paucity of data on the influence of OXT on cell proliferation of corticotroph adenomas. This study aimed to examine whether OXT affects cell growth in pituitary tumor cell lines (AtT20 and GH3 cells) with a focus on corticotroph adenoma cells.METHODS:
Reverse transcription polymerase chain reaction and enzyme-linked immunosorbent assay were conducted with AtT20 cells to confirm the effects of OXT on hormonal activity; flow cytometry was used to assess changes in the cell cycle after OXT treatment. Moreover, the impact of OXT on proliferating cell nuclear antigen (PCNA), nuclear factor κB, and mitogen-activated protein kinase signaling pathway was analyzed by Western blot.RESULTS:
OXT treatment of 50 nM changed the gene expression of OXT receptor and pro-opiomelanocortin within a short time. In addition, OXT significantly reduced adrenocorticotropic hormone secretion within 1 hour. S and G2/M populations of AtT20 cells treated with OXT for 24 hours were significantly decreased compared to the control. Furthermore, OXT treatment decreased the protein levels of PCNA and phosphorylated extracellular-signal-regulated kinase (P-ERK) in AtT20 cells.CONCLUSION:
Although the cytotoxic effect of OXT in AtT20 cells was not definite, OXT may blunt cell proliferation of corticotroph adenomas by altering the cell cycle or reducing PCNA and P-ERK levels. Further research is required to investigate the role of OXT as a potential therapeutic target in corticotroph adenomas.Key words
Full text:
1
Index:
WPRIM
Main subject:
Phosphotransferases
/
Pituitary Neoplasms
/
Protein Kinases
/
Pro-Opiomelanocortin
/
Enzyme-Linked Immunosorbent Assay
/
Oxytocin
/
Gene Expression
/
Cell Cycle
/
Cell Line
/
Blotting, Western
Language:
En
Journal:
Endocrinology and Metabolism
Year:
2019
Type:
Article