Influence of suppression of CapG gene expression by siRNA on the growth and metastasis of human prostate cancer cells

Abstract

ABSTRACT. This study investigated CapG gene expression in prostate cancer cell lines; in addition, we explored the effects of CapG suppression on DU145 cell growth, and the underlying mechanism with which CapG affects DU145 cell growth and invasiveness. The expression of CapG and 18 related genes in DU145 cells was analyzed by flow cytometry, quantitative polymerase chain reaction (qPCR), CCK8 assay, western blot, and the trans-well assay. DU145 cells were transfected with designed small interfering RNA (siRNA). CapG expression was quantified by qPCR and western blot. DU145 cell proliferation and invasiveness was analyzed using the CCK8, flow cytometric, and trans-well assays. CapG, TMPRSS1, EGFR, ETS-1, ERBB2, AKT, Cyclin D1, P21, Bcl-2, and Bak1 gene and Bcl-2, Cyclin D1, and CapG protein expressions were significantly lower in the siRNA group compared to the negative control group (P < 0.05). The proliferation of CapG siRNA DU145 cells was lower than that of the two control groups, 48 h after transfection. The cell inhibition rate was 24.5, 35.4, and 16,5% at 24, 48, and 72 h, respectively. The growth curve indicated that CapG siRNA DU145 cells showed a significantly slower 15769-15778 (2015) proliferation rate (P < 0.05). The trans-well assay showed a significant decrease in the migratory and invasive capacities of DU145 cells in the siRNA group (P < 0.05). The suppression of CapG expression caused a significant decrease in the proliferation, invasiveness, and metastasis of DU145 cells. The mechanism with which CapG, with other oncogenes, influences cancer cell cycle remains to be elucidated.

Cardiovascular Risk Factors and Differential Transcriptomic Profile of the Subcutaneous and Visceral Adipose Tissue and Their Resident Stem Cells

“…capping actin protein (CAPG) is also more highly expressed in SAT than in VAT. CAPG is a member of the gelsolin family, with an important role in endothelial and fibroblast cell motility as well as in macrophage conservation [ 58 , 59 ]. The inflammatory pathway was also differentially regulated between both tissues, higher levels of CD68, a monocyte and macrophage surface marker, were observed in SAT compared with VAT, as well as increased expression of the interferon-gamma-inducible protein 30 (IFI30), expressed by macrophages [ 60 ] and tenascin-C (TNC), protein with roles both in inflammation and in cell migration and proliferation [ 61 , 62 ].…”

MicroRNA and protein profiles in invasive versus non-invasive oral tongue squamous cell carcinoma cells in vitro

“…Recently, CAPG has also shown promise as a potential biomarker for breast cancer [9] and breast cancer metastasis in bone [60]. CAPG silencing by siRNA was shown to decrease proliferation, invasiveness and metastasis of a prostate cancer cell line DU 145 [30], and CAPG has been implicated also in ovarian cancer migration and/or invasion [11,12,66]. However, our current in vitro results indicated that, miR-940 does not regulate CAPG expression in HSC-3 cells invasion or migration in the present study set-ups and under these circumstances.…”

“…Since miR-940 and Macrophage-capping protein (CAPG) pair seemed the most promising candidate miRNA-target gene pair based on bioinformatics (please see the Results section) and recent literature [9,11,12,30,60,66], our aim was to verify if CAPG expression was affected by miR-940 silencing. As the original expression differences were observed in invading HSC-3 cells, two approaches in which the silenced anti-miR-940 HSC-3 cells were either invading or migrating were used to study the miR-940 -CAPG interaction.…”

Progress in Delivery of siRNA-Based Therapeutics Employing Nano-Vehicles for Treatment of Prostate Cancer

“…Taking everything into account, these studies are in line with the fact that dynamic and complicated molecular signaling pathways contribute to the malignant behavior of PCa cells [ 110 , 111 ]. The first step is the recognition of these identified molecular pathways and the additional research being undertaken to identify more molecular pathways involved in PCa malignancy [ 112 , 113 , 114 ]. The next step is designing specific and efficacious siRNAs for targeting the identified molecular signaling pathways for PCa therapy ( Figure 3 ) [ 114 , 115 ].…”