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VEGFC inhibition reverses resistance of bladder cancer cells to cisplatin via upregulating maspin

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The aim of the current study was to elucidate the association between vascular endothelial growth factor C (VEGFC) and resistance of bladder cancer cells to cisplatin and the underlying mechanism involving maspin. A total of 32 bladder cancer tissue samples from patients (18 males and 14 females with an average age of 65.9 years) were collected from the Fifth Affiliated Hospital of Zhengzhou University (Zhengzhou, China). All patients had undergone cisplatinbased combination chemotherapy. In addition, the BIU87 human bladder cancer cell line was cultured and a cisplatinresistant subline (BIU87CisR) was established by continuous exposure to cisplatin. The mRNA expression levels of VEGFC and maspin in tissue samples, BIU87 cells and BIU87CisR cells were analyzed by reverse transcriptionquantitative polymerase chain reaction (RTqPCR). Targeted inhibition of VEGFC in BIU87CisR cells was performed using small interfering (si)RNA technology and the alteration in levels of maspin was confirmed by RTqPCR and western blot analysis. siRNAtreated and untreated BIU87CisR cells were divided into the following four groups: Control group (no drug treatment), 3 µM cisplatin treated group, 3 µM cisplatin + siRNA treated group and the siRNA treated group. Cell viability following treatment in each group was evaluated by the cell counting kit 8 assay. The cell cycle and apoptotic rate of BIU87CisR cells was analyzed by propidium iodide (PI) staining and Annexin VPI double staining with flow cytometry. Furthermore, pcDNAmaspin transfected BIU78CisR cells were used to establish the effect of maspin on the sensitivity to cisplatin. VEGFC expression in chemoresistant patients and BIU87CisR cells was significantly increased compared with chemosensitive patients and normal BIU87 cells, respectively. By contrast, maspin levels were lower in chemoresistant patients and BIU87CisR cells. Subsequent to VEGFC inhibition, maspin expression was markedly increased. Cisplatin (3 µM) resulted in moderate proliferation inhibition of BIU87CisR cells without siRNA pretreatment; however, significant inhibition was observed in the VEGFC siRNA treated group. In addition, the cell cycle arrest and apoptosis induced by cisplatin was enhanced by VEGFC inhibition. Overexpression of maspin was able to improve the sensitivity of BIU87CisR cells to cisplatin. In conclusion, the resistance of bladder cancer cells to cisplatin may be induced by upregulation of VEGFC, and inhibition of VEGFC reverses resistance by elevating maspin expression levels.
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Document Type: Research Article

Affiliations: Department of Urinary Surgery, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450000, P.R. China

Publication date: August 1, 2015

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  • Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
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