Qian-Yuan Zhuang

Tongji Hospital, Wuhan, Hubei, China

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Publications (10)4.6 Total impact

  • Article: Over-expression of LRIG3 suppresses growth and invasion of bladder cancer cells.
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    ABSTRACT: The purpose of this study was to investigate the impact of leucine-rich repeats and immunoglobulin-like domains 3 (LRIG3) on the biological features of bladder cancer cell lines. The plasmids of over-expressed LRIG3 and the blank plasmid serving as control were transfected into the bladder cancer cell lines, T24, EJ and BIU-87, and the expression levels of LRIG3 mRNA and protein were detected by using real-time PCR and Western blotting. The changes in the cell cycle and apoptosis were examined by using flow cytometry. The invasive ability was measured by Transwell assay, and CCK-8 assays were used to measure the proliferation of cells. As compared with the control group, the LRIG3 mRNA and protein expression levels in LRIG3 cDNA-transfected group were raised significantly (P<0.05). The average number of cells with up-regulated LRIG3 passing through the inserted filter was decreased significantly as compared with the control group (P<0.05). Up-regulation of LRIG3 also could inhibit proliferation and induce apoptosis of T24, EJ and BIU-87 cells. Except BIU-87, the T24 and EJ cells transfected with LIRG3 cDNA were arrested in G(0)/G(1) phase compared to the control group (P<0.05). In conclusion, the over-expression of LRIG3 could influence the cell cycle and invasion, inhibit proliferation and induce apoptosis in the three bladder cancer cell lines.
    Journal of Huazhong University of Science and Technology 02/2013; 33(1):111-6. · 0.38 Impact Factor
  • Article: Does urothelial cancer of bladder behave differently in young patients?
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    ABSTRACT: Bladder urothelial cancer has been diagnosed at an increasing rate among young adults in China while the clinical outcomes remain highly controversial. To optimize the management of young patients with bladder cancer, we examined whether bladder urothelial cancer in young patients behaved differently from that in the elder patients. From 1994 to 2008, a database of bladder urothelial cancer patients at a major tertiary medical center was retrospectively reviewed. The clinical and pathological parameters of patients who were less than 40 years of age and a series of patients older than 40 years of age as the control group during the same period were compared. A survival analysis was performed using the Kaplan-Meier method and log-rank test, and Cox regression was performed to identify clinical parameters that affected the clinic outcomes. Young bladder cancer patients had a lower male-to-female ratio and were less likely to have advanced stages and high-grade cancers at the initial diagnosis. Tumors in young bladder cancer patients tended to be less multifocal at diagnosis. In addition, young patients had a lower recurrence rate and longer recurrence interval than older patients. The Kaplan-Meier curve and Log-rank test showed that young patients had significantly better cancer specific survival than old patients. The univariate and multivariate Cox regression analysis revealed that tumor grade is the sole predictor for tumor recurrence in young patients. Young patients with bladder cancer have favorable pathological features and clinical outcomes than older patients. These findings argue for more conservative management approaches for young patients with bladder cancer.
    Chinese medical journal 08/2012; 125(15):2643-8. · 0.86 Impact Factor
  • Article: Small cell carcinoma of the urinary bladder: Three cases report
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    ABSTRACT: Objective: To study the clinical features of patients with primary small cell carcinoma (SCC) of the bladder and to improve the diagnosis and treatment. Methods: Clinical data of 3 cases with primary SCC of the bladder were discussed and the pathology, diagnosis, treatment and prognosis were reviewed. Results: 3 cases of primary SCC of the bladder were presented. Of them the diagnosis was confirmed by pathological examination after operation (2 cases) and biopsy (1 case). One case with stage T4M1 died after three months’ chemotherapy. One case with stage T2M0 underwent partial cystectomy and was treated with chemotherapy and one year later died of miocardial infarction. Another case with stage T4M0 underwent radical cystectomy and postoperative irradiation therapy. The patient was alive and had no recurrence of symptoms during two years follow-up. Conclusion: Primary SCC of the urinary bladder is highly malignant. Radical cystectomy combined with radiotherapy appears to be the efficient treatment. Chemotherapy seems to be of no significant effect.
    Chinese Journal of Cancer Research 05/2012; 16(2):154-156. · 0.18 Impact Factor
  • Article: [Clinical features on chromophobe renal cell carcinoma].
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    ABSTRACT: To explore the clinical, pathological features and prognosis of patients with chromophobe renal cell carcinoma. From January 1998 to January 2008, clinical data of 29 patients with chromophobe renal cell carcinoma including clinical manifestations, imaging examinations, treatment models, pTNM stages and follow-up results, were summarized to investigate its features and prognosis. All cases had no obvious clinical and preoperative imaging presentation. There were 23 patients underwent radical nephrectomy, and 6 cases underwent nephron sparing surgery. Postoperative pathological findings confirmed the diagnosis of chromophobe renal cell carcinoma. Macroscopically, the cut surface of the tumors were generally beige in color. Histologically, it showed polygonal chromophobe cells and small round eosinophilic cells with eccentric hyaline degeneration. These tumor cells had a clear and sharp membrane, lightly stained abundant cytoplasm with a fine reticular translucent pattern and irregular nuclei. And a perinuclear halo was often seen in these cells. Histochemically, the tumor cells generally show a diffuse and strong reaction for CK-8 with a negative expression of Vimentin. The pTNM stages of the tumor were as follows, pT1N0M0 in 11 cases, pT2N0M0 in 8 cases, pT3aN0M0 in 5 cases, pT1N1M0 in 3 cases, pT2N1M0 in 2 cases. Twenty-six cases of patients were followed up (24 to 144 months, with an average of 90 months), 3 cases died of cardio-cerebrovascular disease, and local recurrence involved in 6 cases with reoperation in 4 cases, as well as distant metastasis in 1 case. Twenty-one cases survived with tumor-free. The statistical results indicated that the survival rates of the patients with chromophobe renal cell carcinoma in five years and ten years were 83.9%, 77.9%, respectively, compared with renal cell carcinoma of the same stage 63.8% and 49.9% at the same periods, and there is no difference in the survival rate of five years (P > 0.05) but significant difference in that of ten years (P < 0.01). Chromophobe renal cell carcinoma is a morphologically uncommon subtype of renal cell carcinoma with the good prognosis. Definite diagnosis depends on its typical pathological feature. Radical nephrectomy is the first choice for the treatment of chromophobe renal cell carcinoma.
    Zhonghua wai ke za zhi [Chinese journal of surgery] 04/2011; 49(4):320-3.
  • Article: Rapamycin regulates Akt and ERK phosphorylation through mTORC1 and mTORC2 signaling pathways.
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    ABSTRACT: Numerous studies have shown that mammalian target of rapamycin (mTOR) inhibitor activates Akt signaling pathway via a negative feedback loop while inhibiting mTORC1 signaling. In this report, we focused on studying the role of mTORC1 and mTORC2 in rapamycin-mediated Akt and ERK phosphorylation, and the antitumor effect of rapamycin in cancer cells in combination with Akt and ERK inhibitors. Moreover, we analyzed the effect of mTORC1 and mTORC2 on regulating cell cycle progression. We found that low concentrations rapamycin increased Akt and ERK phosphorylation through a mTORC1-dependent mechanism because knockdowned raptor induced the activation of Akt and ERK, but higher doses of rapamycin inhibited Akt and ERK phosphorylation mainly via the mTORC2 signaling pathway because that the silencing of rictor led to the inhibition of Akt and ERK phosphorylation. We further showed that mTORC2 was tightly associated with the development of cell cycle through an Akt-dependent mechanism. Therefore, we combined PI3K and ERK inhibitors prevent rapamycin-induced Akt activation and enhanced antitumor effects of rapamycin. Collectively, we conclude that mTORC2 plays a much more important role than mTORC1 in rapamycin-mediated phosphorylation of Akt and ERK, and cotargeting AKT and ERK signaling may be a new strategy for enhancing the efficacy of rapamycin-based therapeutic approaches in cancer cells.
    Molecular Carcinogenesis 06/2010; 49(6):603-10. · 3.16 Impact Factor
  • Article: [Effects of B7-H1 blockade on biologic activity of CD3AK cells in vitro].
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    ABSTRACT: To investigate the effect of B7-H1 blockade on proliferation, activation, and antitumor immunity of CD3AK cells. CD3AK cells were induced by stimulation of normal human peripheral blood lymphocytes with CD3 mAbs. Then the cells were cultured with anti-B7-H1 mAbs to block B7-H1 pathway. The proliferation efficiency of CD3AK cells was measured by 3H-thymidine incorporation assay and the concentrations of IFN-gamma, TNF-alpha and IL-10 were measured by ELISA method. Meanwhile the killing activity of CD3AK cells on bladder cancer cell line BIU-87 was measured by MTT method. Blockade of B7-H1 greatly promoted the proliferation of CD3AK cells and extended the survival time of CD3AK cells in vitro. It also enhanced IFN-gamma, TNF-alpha secretion but suppressed IL-10 secretion. And the cytotoxic effect of CD3AK cells on BIU-87 cells were significantly enhanced. Blockade of B7-H1 can promote and retain the proliferation and activation of CD3AK cells. It can also improve the antitumor immunity mediated by CD3AK cells. The manipulation of B7-H1 may become a beneficial target for immunotherapy in tumors.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 09/2009; 25(8):671-3.
  • Article: [Effects of rapamycin on prostate cancer PC-3 cells].
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    ABSTRACT: The mammalian target of rapamycin (mTOR) signaling network regulates cell growth, proliferation, survival and apoptosis. This study was to investigate the effect and the underlying mechanism of rapamycin on prostate cancer PC-3 cells. PC-3 cells were treated with 1 nmol/L rapamycin. The proliferation of PC-3 was examined by MTT. The cell cycle distribution of PC-3 was measured by FCM. The protein levels of raptor, rictor, Akt, pS6k1-T389, pAkt-s473 in PC-3 were examined by western blot. Rapamycin increased the proliferation of PC-3 at 24 h, however, it remarkably inhibited cell proliferation after 36 h (P<0.01), which became more obviously at 72 h. Although incubation with rapamycin slightly induced cell arrest at the S phase at 24 h, this gradually increased PC-3 cells at the G1 phase at 36 h and 48 h. Compared with the control group, the protein levels of raptor and pS6k1-T389 were significantly decreased (P<0.01), and those of rictor and Akt remained unchanged after the treatment with rapamycin for 24 h; the protein level of pAkt-s473 was significantly increased at 24 h (P<0.01), but was obviously inhibited at 36 h and almost completely inhibited at 72 h (P<0.01). Prolonged rapamycin treatment inhibits the proliferation of PC-3 cells. This may be caused by rapamycin-induced cell cycle arrest at the G(1) phase and inhibition of Akt phosphorylation.
    Ai zheng = Aizheng = Chinese journal of cancer 08/2009; 28(8):851-5.
  • Article: [The mTOR inhibitor enhances chemosensitivity of androgen-independent prostate cancer cell line].
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    ABSTRACT: To investigate the effect of the mammalian target of rapamycin (mTOR) inhibitor CCI-779 on the chemosensitivity of androgen-independent prostate cancer cell line PC-3. Prostate cancer cells PC-3 were cultured and treated with CCI-779, Paclitaxel and combination of the two. Then the inhibitory effects of the three medications on the growth of the PC-3 cells were determined by MTT, and the their cell cycle and apoptosis were detected by flow cytometry. Compared with the control group, the three medications all significantly inhibited the proliferation of the PC-3 cells, and the combined method even enhanced the effect. Flow cytometry showed that CCI-779 and Paclitaxel blocked the cell cycle mainly in the G1/G2 stage, while the combined medication mainly in the G0/G1 stage. Significantly increased apoptosis of the PC-3 cells was observed in the three medication groups as compared with the control group (P < 0.01). CCI-779 can inhibit the proliferation of PC-3 cells and enhance the chemosensitivity of prostate cancer.
    Zhonghua nan ke xue = National journal of andrology 07/2009; 15(7):617-20.
  • Article: [Antisense RNA of survivin gene enhances the taxol-induced apoptosis and sensitivity to chemotherapy drugs in bladder cancer cells: an in vitro experiment].
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    ABSTRACT: To evaluate the effects of antisense oligodeoxynucleotide (ASODN) of survivin gene on taxol-induced apoptosis in bladder cancer cells. A survivin ASODN eukaryotic vector pcDNA3-SVVas was transfected into human bladder cancer cells of the line BIU87 mediated by liposomal reagent (BIU87 SVVas cells). The mRNA expression of survivin was measured by RT-PCR. Blank plasmid pcDNA3 was transfected as control (BIU87 neo cells). The cell growth curve was drawn using trypan blue dye exclusion assay. MTT assay was used to investigate the sensibility of transfected cells to taxol. The BIU87 SVVas cells, BIU87 neo cells, and BIU87 cells were cultured in the culture fluid with taxol and then DNA gel electrophoresis, Hoechst nuclear staining and fluorescent microscopy, and annexin-propidium iodide (PI) staining were used to examine the cell apoptosis. Compared to BIU87 and BIU87 neo cells, the mRNA expression of survivin in the BIU87-SVVas cells was obviously reduced. The growth of the BIU87-SVVas cells was significantly reduced in comparison with the BIU87 (P < 0.05). The sensibility of BIU87 SVVas cells to taxol increased significantly shown by cell proliferation and MTT assays. Agarose gel electrophoresis of genomic DNA showed typical DNA ladder only in the BIU87 SVVas cells, but not in other cells. Hoechst nuclear staining and fluorescent microscopy showed that the nuclei of the BIU87 SVVas cells become condense. Annexin-PI test showed that the cell apoptosis rate of the BIU87-SVVas cells treated with taxol was significantly higher than those of the other groups. survivin antisense RNA enhances the taxol-induced apoptosis in the bladder cancer cells. This may lay an experimental foundation for further research of biotherapy in bladder cancer.
    Zhonghua yi xue za zhi 02/2007; 87(6):419-22.
  • Article: [Value of quantitative examination of urine MUC1 in bladder transitional cell carcinoma].
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    ABSTRACT: To evaluate the value of quantitative examination of MUC 1 in the urine of patients with bladder transitional cell carcinoma (BTCC). Urine samples were obtained from 31 patients with BTCC for quantification of MUC 1 content by immunoradiometric analysis. The urine samples were also examined in 10 patients with cystitis glandularis, 10 with benign urine disease and 10 healthy volunteers. The differences in urine MUC1 content were statistically measured between the groups, between cancer patients of different clinical stages and classes, between primary and recurrent cancer patients, and between measurements taken before and after operation. Urine MUC 1 was detected in all the patients. No significant differences were found between the groups, nor between patients with BTCC in all stages (P>0.05), or between primary and recurrent cancer patients (P>0.05). But MUC 1 contents showed significant difference before and after the operation in the cancer patients (P<0.05). Urine MUC 1 can not serve as the marker to screen and diagnose BTCC, but it can be useful in therapeutic effect and prognostic evaluation. Specific oncogene markers are more significant than oncogene phenotype markers in clinical diagnosis and screen of BTCC.
    Di 1 jun yi da xue xue bao = Academic journal of the first medical college of PLA 08/2005; 25(8):998-1000.