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Gene expression profile of STAT3 in ovarian cancer cell (SKOV3ip1)

ABSTRACT: RNA interference (RNAi) holds tremendous potential as a therapeutic approach, especially in the treatment of malignant tumors. However, efficient and biocompatible delivery methods are needed for systemic delivery of siRNA. To achieve this goal, we have established a novel formulation of siRNA by incorporating it into reconstituted high density lipoprotein (rHDL) nanoparticles. Here, we demonstrate that rHDL nanoparticles facilitate highly efficient systemic delivery of siRNA in vivo, mediated by the scavenger receptor type B1 (SR-B1). Moreover, in therapeutic proof-of-concept studies, these nanoparticles were effective in targeting either signal transducer and activator of transcription 3 (STAT3) or focal adhesion kinase (FAK) expression in orthotopic mouse models of ovarian and colorectal cancer. These data indicate that an rHDL nanoparticle is a novel and highly efficient siRNA carrier, and therefore this novel technology could serve as the foundation for new cancer therapeutic approaches.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20597 | GEO | 2011/12/22

SECONDARY ACCESSION(S): PRJNA124883

REPOSITORIES: GEO

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Gene expression profile of STAT3 in ovarian cancer cell (SKOV3ip1)

Project description:RNA interference (RNAi) holds tremendous potential as a therapeutic approach, especially in the treatment of malignant tumors. However, efficient and biocompatible delivery methods are needed for systemic delivery of siRNA. To achieve this goal, we have established a novel formulation of siRNA by incorporating it into reconstituted high density lipoprotein (rHDL) nanoparticles. Here, we demonstrate that rHDL nanoparticles facilitate highly efficient systemic delivery of siRNA in vivo, mediated by the scavenger receptor type B1 (SR-B1). Moreover, in therapeutic proof-of-concept studies, these nanoparticles were effective in targeting either signal transducer and activator of transcription 3 (STAT3) or focal adhesion kinase (FAK) expression in orthotopic mouse models of ovarian and colorectal cancer. These data indicate that an rHDL nanoparticle is a novel and highly efficient siRNA carrier, and therefore this novel technology could serve as the foundation for new cancer therapeutic approaches. To identify the role of STAT3 in ovarian cancer cell, we performed microarray after knocking down STAT3 in ovarican cancer cells (3 siCon and 3 siSTAT3).

2011-12-22 | E-GEOD-20597 | biostudies-arrayexpress

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Homo sapiens

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Project description:The current standard-of-care for advanced liver cancer is limited. Therefore, there is an urgent need for development of novel molecular targeted therapy. Increase of WEE1 kinase activity through an epigenetic regulation plays an important role in the development of hepatocellular carcinoma (HCC). Here we demonstrated that WEE1 siRNA silencing caused inhibition of HCC cell growth through blockade of cell cycle progression and induction of apoptosis. The anti-proliferative effects were driven by a subset of molecular alterations including the upregulation of cdk inhibitor p21 and the downregulation of AKT1, CDK2, cyclin B1 (CCNB1), PARP1 and GPAM which are functionally involved in control of cell cycle, apoptosis and lipid metabolism. Systemic delivery of a modified WEE1 siRNA encapsulated in lipid nanoparticles significantly inhibited human HCC growth in murine xenograft models, and increased mice survival. Wee1 silencing in tumor cells also resulted in a strong inhibition of lipogenesis (SREBP1C, FAS) and caused a marked decrease in fat accumulation. Of importance, knockdown of WEE1 dramatically reduced the portion of liver cancer stem cells (CSCs) population through co-downregulation of cancer stemness genes and weakened the capacity of sphere formation and the ability of cancer cell migration. Our findings suggest that the epigenetic modifier WEE1 functionally involve to HCC lipid metabolism and CSC-like phenotype maintenance and that molecular targeting of WEE1 may be an effective systemic therapy for prevention of tumor recurrence via elimination of CSCs in liver tumor microenvironment.

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