期刊
CANCERS
卷 15, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/cancers15010237
关键词
therapeutic device; ovarian cancer; tumor growth
类别
Honeycomb-like structured films (HCFs), as three-dimensional porous scaffolds, can inhibit the growth, differentiation, proliferation, and motility of ovarian cancer cells by inducing abnormal focal adhesion and morphological changes, providing a novel device for inhibiting residual tumor growth after surgery and improving the prognosis for patients with advanced ovarian cancer.
Simple Summary Ovarian cancer cell dissemination can lead to inoperability and death in patients with advanced ovarian cancer. Honeycomb-like structured films (HCFs) are three-dimensional (3D) porous scaffolds fabricated from biodegradable polymers and have been widely used in tissue engineering. We assessed whether HCFs could be a novel strategy to inhibit residual tumor growth after surgery. Here, we show that HCFs can remarkably suppress tumor growth in an in vivo ovarian cancer model. RNA sequencing of paired tumors treated with HCFs and control tumors that were treated without films demonstrated that HCFs induced abnormal focal adhesion and cell morphological change, subsequently inhibiting differentiation, proliferation and motility in ovarian cancer cells. Our data suggest that HCFs could inhibit residual tumor growth after surgery, reduce surgical invasiveness, and improve prognosis for patients with advanced ovarian cancer. Ovarian cancer cell dissemination can lead to the mortality of patients with advanced ovarian cancer. Complete surgery for no gross residual disease contributes to a more favorable prognosis than that of patients with residual disease. HCFs have highly regular porous structures and their 3D porous structures act as scaffolds for cell adhesion. HCFs are fabricated from biodegradable polymers and have been widely used in tissue engineering. This study aimed to show that HCFs suppress tumor growth in an in vivo ovarian cancer model. The HCF pore sizes had a significant influence on tumor growth inhibition, and HCFs induced morphological changes that rounded out ovarian cancer cells. Furthermore, we identified gene ontology (GO) terms and clusters of genes downregulated by HCFs. qPCR analysis demonstrated that a honeycomb structure downregulated the expression of CXCL2, FOXC1, MMP14, and SNAI2, which are involved in cell proliferation, migration, invasion, angiogenesis, focal adhesion, extracellular matrix (ECM), and epithelial-mesenchymal transition (EMT). Collectively, HCFs induced abnormal focal adhesion and cell morphological changes, subsequently inhibiting the differentiation, proliferation and motility of ovarian cancer cells. Our data suggest that HCFs could be a novel device for inhibiting residual tumor growth after surgery, and could reduce surgical invasiveness and improve the prognosis for patients with advanced ovarian cancer.
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