Objective  Delta Np63 (ΔNp63) is a nuclear transcription factor that maintains epithelial progenitor cell populations

and is over-expressed in several epithelial cancers. However

the expression of ΔNp63 in transitional cell carcinoma of the bladder (TCCB) is still disputable

and the mechanisms by which ΔNp63 p

romotes cell survival are unclear. To explore the inhibitory effect of tumor growth and cyclin D

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expression by silencing   ΔNp63 with short hairpin RNA (shRNA) on human TCCB in xenograft nude mice. Methods  Human TCCB 5637 cells were transplanted into nude mice to establish xenograft tumors. ΔNp63 specific shRNA expression plasmid was constructed and then transfected into the tumor masses. The tumor volume was observed

tumor morphology with HE staining

and ultramicrostructure with transmission electron microscopy. The inhibitory effect of ΔNp63 was studied with semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). Protein expressions of ΔNp63

proliferation cell nuclear antigen (PCNA) and cyclin D

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were examined with the immunohistochemical staining assay. Results  After 8 weeks of the transfection of ΔNp63 specific shRNA plasmid

the tumor volume was significantly smaller in ΔNp63 shRNA group than in control shRNA and normal saline group (P0.01)

with an inhibitory rate of 74.44% in ΔNp63 shRNA group

and no significant difference was seen between control shRNA and normal saline group (P0.05). In ΔNp63 shRNA group

the necrosis and decrease of karyokinesis were observed under light microscope and transmission electron microscope

and apoptosis and inflammatory cells were also found under transmission electron microscope. There was no such change seen in control shRNA and normal saline groups. ΔNp63 shRNA directly down-regulated the expressions of delta Np63 protein and mRNA

and the protein expression of PCNA and cyclin D

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.  Conclusion  The Pgenesil-1ΔNp63 shRNA plasmid significantly inhibits the growth of TCCB in nude mice

and suppresses the cellular proliferation of TCCB through inhibiting cyclin D

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expression.