Journal
EXPERIMENTAL HEMATOLOGY & ONCOLOGY
Volume 11, Issue 1, Pages -Publisher
BMC
DOI: 10.1186/s40164-022-00358-y
Keywords
Sphingosine kinase 1 (SphK1); Adipocyte; Ovarian cancer; Metastasis
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]
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In this study, it was found that SphK1 is over-expressed in omental metastases of EOC patients. The inhibition of SphK1 suppressed the metastatic ability of EOC induced by adipocytes. SphK1 modulates adipocyte-induced E/N-cadherin switch through Twist1, suggesting a new target for EOC therapy.
Unlike many solid tumors, epithelial ovarian cancer (EOC) has a clear metastatic predilection to the adipocyte-rich niche, especially the omentum. However, the underlying mechanism driving this process remains incomplete. Here we show that SphK1 is over-expressed in omental metastases compared with ovarian primary tumors in EOC patients. In vitro, inhibition of SphK1 suppressed the metastatic ability of EOC induced by adipocytes. In vivo, blockage of SphK1 could attenuate the omental metastasis of EOC. Importantly, SphK1 modulates adipocyte-induced E/N-cadherin switch through Twist1, a key process in EOC metastasis. Our study reveals a previously unrecognized role of SphK1 in modulating the metastatic tropism of EOC to the adipocyte-rich niche, suggesting a new target for EOC therapy.
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