Chondroitin Sulfate Proteoglycan 4 Provides New Treatment Approach to Preventing Peritoneal Dissemination in Ovarian Cancer.
Kaname UnoYoshihiro KoyaMasato YoshiharaShohei IyoshiKazuhisa KitamiMai SugiyamaEmiri MiyamotoKazumasa MogiHiroki FujimotoYoshihiko YamakitaXinhui WangAkihiro NawaHiroaki KajiyamaPublished in: International journal of molecular sciences (2024)
Most epithelial ovarian cancer (EOC) patients are diagnosed with peritoneal dissemination. Cellular interactions are an important aspect of EOC cells when they detach from the primary site of the ovary. However, the mechanism remains underexplored. Our study aimed to reveal the role of chondroitin sulfate proteoglycan 4 (CSPG4) in EOC with a major focus on cell-cell interactions. We examined the expression of CSPG4 in clinical samples and cell lines of EOC. The proliferation, migration, and invasion abilities of the CSPG4 knockdown cells were assessed. We also assessed the role of CSPG4 in spheroid formation and peritoneal metastasis in an in vivo model using sh-CSPG4 EOC cell lines. Of the clinical samples, 23 (44.2%) samples expressed CSPG4. CSPG4 was associated with a worse prognosis in patients with advanced EOC. Among the EOC cell lines, aggressive cell lines, including ES2, expressed CSPG4. When CSPG4 was knocked down using siRNA or shRNA, the cell proliferation, migration, and invasion abilities were significantly decreased compared to the control cells. Proteomic analyses showed changes in the expression of proteins related to the cell movement pathways. Spheroid formation was significantly inhibited when CSPG4 was inhibited. The number of nodules and the tumor burden of the omentum were significantly decreased in the sh-CSPG4 mouse models. In the peritoneal wash fluid from mice injected with sh-CSPG4 EOC cells, significantly fewer spheroids were present. Reduced CSPG4 expression was observed in lymphoid enhancer-binding factor 1-inhibited cells. CSPG4 is associated with aggressive features of EOC and poor prognosis. CSPG4 could be a new treatment target for blocking peritoneal metastasis by inhibiting spheroid formation.
Keyphrases
- poor prognosis
- induced apoptosis
- cell cycle arrest
- cell proliferation
- signaling pathway
- long non coding rna
- single cell
- stem cells
- mesenchymal stem cells
- chronic kidney disease
- end stage renal disease
- adipose tissue
- binding protein
- cell therapy
- mouse model
- gene expression
- prognostic factors
- newly diagnosed
- type diabetes
- transcription factor
- metabolic syndrome
- ejection fraction
- dna methylation
- bone marrow
- patient reported outcomes
- drug induced