Abstract
ObjectiveTo investigate the detailed roles and mechanisms of tumor-derived exosomes in progression and metastasis of ovarian cancer in vitro.MethodsExosomes were isolated by differential centrifugation method; the morphology, size and biological markers of exosomes were separately defined by transmission electron microscopy, nanoS90 and Western blotting; Trans-well chambers assay was used to assess the ability of migration and invasion of recipient cells uptaking the exosomes from HO8910PM cells. The downstream molecule was screened by mass spectrometry.CD44 was identified by western blotting and the function of CD44 was identified by trans-well chambers assay and CCK8 assay.ResultsExosomes derived from HO8910PM cells could be transferred to HO8910 cells and promote cell migration and invasion in the recipient cells of ovarian cancer. And CD44 could be transferred to the HO8910 cells through exosomes from HO8910PM cells and influence the migration and invasion ability of HO8910 cells.ConclusionThe more aggressive subpopulation can transfer a metastatic phenotype to the less one via secreting exosomes within a heterogeneous tumor. CD44 may be a potential therapeutic approach for ovarian cancer.
Highlights
Ovarian cancer is the most lethal type in gynecological neoplasms
We presented the evidence that exosomes derived from high metastatic ovarian cells can be transferred to low metastatic ovarian cancer cells and promote the migration and invasion of recipient cells
Electron microscopy revealed that both PMExos and HOExos had a round or cup-shaped morphology, with the diameter ranging 50-250 nm for PMExos and 50-200 nm for HOExos, respectively (Fig. 1e). Both exosomes were enriched for exosome markers, including CD63, CD81, CD9 and HSP70 (Fig. 1f), suggesting that both cultured HO8910 and HO8910PM cells possess the ability to release exosomes
Summary
Ovarian cancer is the most lethal type in gynecological neoplasms. The overall 5-year survival rate of ovarian cancer patients was 47% according to cancer. Cancers, including ovarian cancer, frequently display substantial intra-tumor heterogeneity in virtually all distinguishable phenotypic features, such as cellular morphology, gene expression (including the expression of cell surface markers and growth factors and hormonal receptors), metabolism, motility, angiogenic, proliferative, immunogenic, and metastatic potential [9, 11, 17, 28]. Shen et al Journal of Ovarian Research (2021) 14:38. All those heterogeneous cells tend to homogenous in the similiar microenvironment. All cancer cells eventually present similar aggressive potential via intercellular interactions without outside intervention. Understanding the mechanism would help to improve the treatment strategies for cancer
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