Activation of SphK2 contributes to adipocyte-induced EOC cell proliferation

Epithelial ovarian cancer (EOC) is the leading cause of deaths due to cancer in women. Adipocytes have been suggested to play a key role in the stimulation of EOC growth. However, the mechanisms underlying the adipocyte-induced EOC proliferation remain undefined. Here, we provide the first evidence...

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Bibliographic Details
Published in:Open medicine (Warsaw, Poland) Poland), 2022-01, Vol.17 (1), p.229-238
Main Authors: Dai, Lan, Wang, Chen, Wang, Wenjing, Song, Keqi, Ye, Taiyang, Zhu, Jie, Di, Wen
Format: Article
Language:English
Subjects:
Adipocytes
Antibiotics
Antibodies
Biology
Cell cycle
Cell growth
Enzymes
epithelial ovarian cancer
Gynecology
Kinases
Laboratories
Medicine
Metabolism
Obstetrics
Oncology
Ovarian cancer
proliferation
Proteins
sphingosine kinase 2
Tumors
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Summary:Epithelial ovarian cancer (EOC) is the leading cause of deaths due to cancer in women. Adipocytes have been suggested to play a key role in the stimulation of EOC growth. However, the mechanisms underlying the adipocyte-induced EOC proliferation remain undefined. Here, we provide the first evidence that adipocytes induce the activation of sphingosine kinase (SphK) 2 in EOC, which represents a novel pathway that mediates the adipocyte-induced EOC growth. SphK2 inhibition in EOC cells led to a remarkable inhibition of the adipocyte-induced cell proliferation. Moreover, the adipocyte-induced SphK2 activation in EOC cells was extracellular signal-regulated protein kinases (ERK) dependent. Furthermore, silencing SphK2 in EOC significantly inhibited the adipocyte-induced expression of phospho-ERK and c-Myc, two crucial players in EOC growth. Collectively, the current study unraveled a previously unrecognized role of SphK2 in the adipocyte-induced growth-promoting action in EOC, suggesting a novel target for EOC treatment.
ISSN:2391-5463
2391-5463
DOI:10.1515/med-2022-0422