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Publications (5)1.96 Total impact

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    ABSTRACT: The efficacy and specificity of treatment are the major challenges for cancer gene therapy. Oncolytic virotherapy is an attractive drug delivery platform of cancer gene therapy. Previous studies have determined that apoptin is a p53-independent, Bcl-2-insensitive apoptotic protein that has the ability to induce apoptosis specifically in tumor cells. In this study, we show that the administration of a dual cancer-specific oncolytic adenovirus construct, Ad-hTERT-E1a-apoptin [in which the adenovirus early region 1a (E1a) gene is driven by the cancer-specific promoter of human telomerase reverse transcriptase (hTERT) and that expresses apoptin simultaneously], suppresses tumor growth in gastric carcinoma cells in vitro and reduces the tumor burden in vivo in xenografted nude mice. The observation that infection with the Ad-hTERT-E1a-apoptin construct significantly inhibited the growth of gastric cancer cells and protected normal human gastric epithelium from growth inhibition confirmed the induction of cancer cell-selective adenovirus replication, growth inhibition and apoptosis by this therapeutic approach. In vivo assays were performed using BALB/c nude mice that had established primary tumors. Subcutaneous primary tumor volume was reduced not only in the intratumoral injection group but also in the systemic delivery mice following treatment with Ad-hTERT-E1a-apoptin. Furthermore, treatment of primary models with Ad-hTERT-E1a-apoptin increased the mouse survival time. These data reinforce previous research and highlight the potential therapeutic application of Ad-hTERT-E1a-apoptin for the treatment of neoplastic diseases in clinical trials.
    International Journal of Molecular Medicine 07/2012; · 1.96 Impact Factor
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    ABSTRACT: To observe the therapeutic effect of tympanoplasty with soft-wall reconstruction of ear canal for chronic otitis media with cholesteatoma. Seventy-three patients (76 ears) suffering from chronic otitis media with cholesteatoma were treated with canal wall down mastoidectomy with tympanoplasty. Postauricular myo-periosteal flap was used to the soft-wall reconstruction of ear canal, and the cavityplasty of auricular concha was not performed. The auricular bone prosthesis was made of the autogeneic mastoid cortical bone or residual incus. The postoperative modality and the function of external auditory canal and the postoperative hearing and the postoperative complications were observed. The mean dry ear time was (21.1 +/- 3. 1) days after surgery in this study. The postoperative modality of external auditory canal was normal on the whole. The patients were followed up between 6 months and 24 months after surgery. The postoperative average air conduction hearing was improved by (14.5 +/- 6.1) dB HL. Tympanoplasty with soft-wall reconstruction of ear canal using the postauricular myo-periosteal flap can recover the modality and function of external auditory canal on the whole, and the cavityplasty of auricular concha is not needed. The postoperative hearing can be improved by this technique satisfactorily.
    Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 08/2011; 25(16):744-6.
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    ABSTRACT: To investigate the anti-tumor effects and the mechanism of the recombinant fowlpox virus expressing Apoptin gene on human laryngeal carcinoma Hep-2. Hep-2 cells cultured in vitro were infected with vFVApoptin. The anti-tumor effects on Hep-2 cells were measured through MTT staining and, the mitochondrial trans-membrane potential (delta psi m) and reactive oxygen species (ROS) were analyzed by flow cytometry. Western blot was used to detect the release of cytochrome c (Cyto c). Caspase-3/9 activities were measured by colorimetric assay. vFVApoptin could restrain Hep-2 cells significantly and, had the function of down-regulating delta psi m, up-regulating ROS, promoting Cyto c release and activating Caspase-3/9. Cyto c were released from mitochondria by the function of up-regulating ROS of vFVApoptin. Cyto c triggered Caspase-9 and, after the activation of Caspase-9, downstream apoptotic factors, such as caspase-3, were activated. Eventually, Hep-2 cells were suppressed by mitochondrial pathway apoptosis induced by vFVApoptin.
    Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 04/2009; 23(6):264-6, 270.
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    ABSTRACT: To study induction of apoptosis and inhibition of proliferation in Hep-2 by survivin gene targeting. Antisense survivin RNA expression vector was constructed and then was transfected to human laryngeal carcinoma cell line Hep-2 by lipofectamine. HpEGFP/survivin cells were abstained by using G418. The level of survivin protein before and after transfection was determined by Western blot. Proliferation activity was measured by MTT assay. The experiment of colony formation in soft agar was carried out. Apoptosis was assessed by flow cytometry and acridine orange (AO). After antisense survivin RNA plasmids were transfected, the level of survivin protein was inhibited in Hep-2. Compared with control, proliferation of HpEGFP/survivin cells transfected with the recombinant of antisense survivin RNA were suppressed significantly. The experiment of colony formation in soft agar showed the ability of colony formation decreased in HpEGFP/survivin cells compared to control (P <0.05). Apoptosis rate increased about 1.81 folds compared with control. The recombination antisense survivin RNA plasmid can partly inhibit the level of survivin protein expression in Hep-2. Antisense survivin RNA can induce apoptosis and inhibit the proliferation of Hep-2 by down-regulating the expression of endogenous survivin in vitro.
    Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 01/2006; 19(24):1138-41.
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    ABSTRACT: To research the antitumor efficacy on mice model bearing H22 tumor with application of pVVP3IL-18HN and its mechanism of the antitumor effect on Hep-2. pVVP3IL-18HN was introduced into Hep-2 cells by liposome, then cellular morphology was observed through AO/EB stain. To evaluate the mechanism of the antitumor effect on Hep-2 of pVVP3IL-18HN and its effect on tumor immunogenicity, flow cytometer (FCM) was used to detect the variation of mitochondrial trans-membrane potential,reactive oxygen species (ROS) and the MHC-I. C57BL/6 mice were subcutaneously inoculated with 2 X 10(5) H22 tumor cells in the right hindlimb, and 7, 14 and 21 day post-inoculation, pVVP3IL-18HN was administrated intratumorally. The pVVP3, pVIL-18, PVHN and PBS control group were treated as above. Then the tumor suppression and specific cytotoxic T lymphocyte (CTL) activity was detected. After the transfection of pVVP3IL-18HN, tumor cells crenated and stained by AO/EB. In the research pVVP3IL-18HN was found to up-regulate the value of ROS and the expression of MHC-I, and down-regulate the value of mitochondrial trans-membrane potential. The tumor suppression rate of pVVP3IL-18HN was 60.5% and a dramatically increased tumor suppression was revealed in the pVVP3IL-18HN treated mice as compared with control mice treated with PBS (P < 0.05). pVVP3IL-18HN kill the tumor cells by apoptosis and have notable antitumor effect in vivo.
    Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 09/2005; 19(15):704-6.