Journal
JOURNAL OF OVARIAN RESEARCH
Volume 14, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s13048-021-00815-y
Keywords
Epithelial ovarian cancer (EOC); Adipocytes; Sphingosine kinase 1 (SphK1); Sphingosine 1-phosphate receptor (S1PR); Proliferation
Categories
Funding
- National Natural Science Foundation of China (NSFC) [81974401, 81974454]
- Science and Technology Commission of Shanghai municipality [18ZR1423100]
- Shanghai Municipal Commission of Health and Family Planning [2017YQ035]
Ask authors/readers for more resources
This study highlights the critical role of SphK1 in adipocyte-induced EOC cell proliferation, involving ERK phosphorylation and the S1PR1 and S1PR3 signaling pathways. The findings suggest a new potential target for EOC therapy.
Background Adipocytes, active facilitators of epithelial ovarian cancer (EOC) growth, have been implicated in the link between obesity and EOC. However, the current understanding of the mechanisms underlying adipocyte-induced EOC cell proliferation remains incomplete. Results We provide the first evidence showing that sphingosine kinase (SphK) 1 is critical for adipocyte-induced EOC cell proliferation. Adipocytes are capable of activating SphK1, which then leads to extracellular signal-regulated kinase (ERK) phosphorylation. Moreover, adipocyte-induced SphK1 activation is ERK dependent. Furthermore, sphingosine 1-phosphate receptor (S1PR) 1 and S1PR3, key components of the SphK1 signalling pathway, participate in adipocyte-mediated growth-promoting action in EOC cells. Conclusions Our study reveals a previously unrecognized role of SphK1 in adipocyte-induced growth-promoting action in EOC, suggesting a new target for EOC therapy.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available