Abstract：
OBJECTIVES:To determine whether platelet-derived growth factor receptor (PDGFR) plays a role in the tumorigenicity of prostate cancer cells. METHODS:PC3 prostate cancer cells were transfected with small interfering (si)PDGFR-α and siPDGFR-β, constructed according to the conventional small interfering RNA design standard. Reverse transcriptase polymerase chain reaction, Western blot analysis, and cell growth were studied to determine the characteristics of PDGFR-α and PDGFR-β in vitro. The prostate cancer xenograft model was established to investigate whether knockout of PDGFR-α and PDGFR-β decreases prostate cancer tumor growth in vivo. The experimental groups were defined as group 1 (PC3 cells only), group 2 (PC3 cells transfected with small interfering green fluorescent protein), group 3 (PC3 cells transfected with siPDGFR-α), group 4 (PC3 cells transfected with siPDGFR-β), and group 5 (PC3 cells transfected with siPDGFR-α and siPDGFR-β). RESULTS:Western blot analysis revealed that siPDGFR-α and siPDGFR-β significantly blocked PDGFR-α and PDGFR-β protein expression. After 48 hours of transfection of the PC3 cells with siPDGFR-α and siPDGFR-β, the relative fractions of viable cells were reduced to 47.7% (P = .007) and 38.5% (P = .010). In vivo, mice treated with siPDGFR-α or siPDGFR-β and siPDGFR-α plus siPDGFR-β had significant tumor cell growth arrest compared with the mice in groups 1 and 2 (P = .001). In addition, a significant reduction in the microvessel density was observed in tumors from the mice treated with siPDGFR-α or siPDGFR-β and siPDGFR-α plus siPDGFR-β (P < .001). CONCLUSIONS:The results of the present study suggest that siPDGFR-α and siPDGFR-β might inhibit prostate cancer cell growth by the suppression of angiogenesis.
journal_name
Urologyjournal_title
Urologyauthors
Park YH,Seo SY,Ha M,Ku JH,Kim HH,Kwak Cdoi
10.1016/j.urology.2011.01.050subject
Has Abstractpub_date
2011-06-01 00:00:00pages
1509.e9-15issue
6eissn
0090-4295issn
1527-9995pii
S0090-4295(11)00124-5journal_volume
77pub_type
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