inhibits invasion of human ovarian cancer cells by affecting cytoskeletal structure and the number of focal adhesion.

BACKGROUND

Ovarian cancer (OV) is associated with the highest mortality rate among gynecological cancers, largely due to late diagnosis and chemoresistance. The identification of novel diagnostic markers and therapeutic targets is crucial. Caldesmon 1 (), a cytoskeleton-regulating protein, has been implicated in various cancers. This study aims to investigate the expression and functional significance of in OV, focusing on its potential impact on cell invasion and metastasis.

METHODS

We analyzed expression using The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) databases, along with tissue microarray immunohistochemistry (IHC). Drug sensitivity analysis was performed using the 'oncopredict' R package. A gene network was constructed, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. SK-OV-3 cell lines with stable knockdown were established and verified by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot (WB). We then assessed cell invasiveness using Transwell assays and visualized cytoskeletal changes through immunofluorescence staining of F-actin and Vinculin.

RESULTS

The expression of was significantly reduced in OV tissues compared to normal tissues. Patients with high and low expression levels of showed significant differences in their response to chemotherapeutic drugs. and its related genes were found to play an essential role in regulating cytoskeleton organization, focal adhesion formation, and cell movement processes. knockdown cells exhibited a significant reduction in F-actin stress fibers, a loose cytoskeleton structure, decreased Vinculin expression, and enhanced migration ability.

CONCLUSIONS

Attenuated expression of in SK-OV-3 cells leads to fewer F-actin stress fibers, reducing the association between the cytoskeleton and Vinculin. This results in reduced cellular focal adhesions and increased invasiveness of SK-OV-3 cells, promoting OV cell metastasis. These findings suggest that may have important clinical implications in the diagnosis and treatment of OV.