Xian-Cheng Chen

Publications of Xian-Cheng Chen

• A novel transdermal plasmid-dimethylsulfoxide delivery technique for treatment of psoriasis.

  Authors: Yan Zhang, Jiong Li, Chang-Yong Liu, Xi-Kun Zhou, Ji Qiu, Yin-Bing Zhang, Nong-Yu Huang, You Li, Xiang-Jun Chen, Xiao-Lei Li, Yong-Sheng Wang, Han-Suo Yang, Xian-Cheng Chen, Bing Kan, Yong-Qiu Mao, Hong-Xin Deng, Li Yang, Yan-Jun Wen, Xia Zhao, Yu-Quan Wei

  Dermatology (Basel, Switzerland). 08/2010; 221(1):84-92.

  Psoriasis is a chronic and relapsing inflammatory skin disease associated with various immunologic abnormalities. Repeated subcutaneous injection of interleukin-4 (IL-4) has been established as anPsoriasis is a chronic and relapsing inflammatory skin disease associated with various immunologic abnormalities. Repeated subcutaneous injection of interleukin-4 (IL-4) has been established as an effective treatment to counteract psoriasis. We investigated whether gene therapy using IL-4 expression plasmid (pIL-4) via transdermal delivery was an alternative treatment for psoriasis. In our experiment, dimethylsulfoxide (DMSO) was used as a penetration enhancer. At first, the penetration efficiency of the complex of reporter plasmid accompanied by DMSO was investigated both in vitro and in vivo. Then, the antipsoriasis efficiency of the treatment with pIL-4-DMSO was tested in mice. The expression of the reporter gene was detected in epidermis and dermis both in vitro and in vivo. More importantly, the psoriasis symptoms were relieved, and significant reductions in some psoriasis-associated factors were observed after pIL-4-DMSO treatment. We conclude that the topical application of pIL-4-DMSO can treat psoriasis to a significant extent.

• Anti-tumor activity of N-trimethyl chitosan-encapsulated camptothecin in a mouse melanoma model.

  Authors: Xian-Ping Liu, Sheng-Tao Zhou, Xing-Yi Li, Xian-Cheng Chen, Xia Zhao, Zhi-Yong Qian, Li-Na Zhou, Zhi-Yong Li, Yu-Mei Wang, Qian Zhong, Tao Yi, Zheng-Yu Li, Xiang He, Yu-Quan Wei

  Journal of experimental & clinical cancer research : CR. 01/2010; 29:76.

  Camptothecin (CPT) has recently attracted increasing attention as a promising anticancer agent for a variety of tumors. But the clinical application is largely hampered by its extreme waterCamptothecin (CPT) has recently attracted increasing attention as a promising anticancer agent for a variety of tumors. But the clinical application is largely hampered by its extreme water insolubility and unpredictable side effect. It is essential to establish an efficient and safe protocol for the administration of CPT versus melanoma. Camptothecin was encapsulated with N-trimethyl chitosan (CPT-TMC) through microprecipitation and sonication. Its inhibition effect on B16-F10 cell proliferation and induction of apoptosis was evaluated by MTT assay and flow cytometric analysis in vitro. The anti-tumor activity of CPT-TMC was evaluated in C57BL/6 mice bearing B16-F10 melanoma. Tumor volume, tumor weight and survival time were recorded. Assessment of apoptotic cells within tumor tissue was performed by TUNEL assay. Antiangiogenesis and antiproliferation effects of CPT-TMC in vivo were conducted via CD31 and PCNA immunohistochemistry, respectively. CPT-TMC efficiently inhibited B16-F10 cells proliferation and increased apoptosis in vitro. Experiment group showed significant inhibition compared with free CPT-treated group (81.3% vs. 56.9%) in the growth of B16-F10 melanoma xenografts and prolonged the survival time of the treated mice (P < 0.05). Decreased cell proliferation, increased tumor apoptosis as well as a reduction in angiogenesis were observed. Our data suggest that N-trimethyl chitosan-encapsulated camptothecin is superior to free CPT by overcoming its insolubility and finally raises the potential of its application in melanoma therapy.

• Antitumor effect of mSurvivinThr34 --> Ala in murine colon carcinoma when administered intravenously.

  Authors: Hong-Xia Li, Xin-Yu Zhao, Lian Wang, Yong-Sheng Wang, Bin Kan, Jian-Rong Xu, Jiong Li, Yan-Jun Wen, Xing-Chen Peng, Xiang Chen, Fei Yan, Bin Ye, Xiao-Bo Du, Ju-Mei Zhao, Tao Yi, Xian-Cheng Chen, Xiao-Xia Du, Yu-Quan Wei, Xia Zhao

  Medical oncology (Northwood, London, England). 12/2009;

  Colorectal cancer is one of the most common cancers. Survivin is strongly immunogenic in a fraction of colorectal cancer patients. The present study was designed to determine whether full-lengthColorectal cancer is one of the most common cancers. Survivin is strongly immunogenic in a fraction of colorectal cancer patients. The present study was designed to determine whether full-length mouse Survivin dominant-negative mutant SurvivinT34A has the antitumor activity in a murine colon carcinoma model. The complex of cationic liposome (DOTAP/Chol) to plasmid pORF9-mSurvivin T34A was administered intravenously in a mouse subcutaneous (S. C.) CT 26 tumor model. Apoptotic cells and anti-angiogenesis were evaluated by fluorescent in situ TUNEL assay and by immunohistochemistry with an antibody reactive to CD31, respectively. A 4 h (51)Cr release assay was performed to determine Survivin-specific cytotoxicity. The adoptive transfer of CD8(+) or CD4(+) T-lymphocytes assay was to further explore the roles of immune cell subsets. We demonstrated the complex of cationic liposome (DOTAP/Chol) to plasmid pORF9-mSurvivin T34A when administered intravenously induced an efficient antitumor activity in a S. C. CT26 tumor model in mice. The main mechanism is involved in three aspects: triggering the apoptosis of tumor cells, inhibiting angiogenesis, and inducing Survivin-specific immune response. Our observations may have potential implications for the further exploration of the treatment of human colorectal cancer by intravenous delivery of dominant-negative mutant Survivin T34A.

• Intratumoral Expression of Mature Human Neutrophil Peptide-1 Mediates Antitumor Immunity in Mice.

  Authors: Yong-Sheng Wang, Dan Li, Hua-Shan Shi, Yan-Jun Wen, Li Yang, Ning Xu, Xian-Cheng Chen, Xiang Chen, Ping Chen, Jiong Li, Hong-Xin Deng, Chun-Ting Wang, Gang Xie, Shan Huang, Yong-Qiu Mao, Li-Juan Chen, Xia Zhao, Yu-Quan Wei

  Clinical cancer research : an official journal of the American Association for Cancer Research. 10/2009;

  PURPOSE: Human neutrophil peptides (HNP1-3), small molecular antimicrobial peptides, are expressed within tumors and associated with tumor necrosis and inhibition of angiogenesis. RecentPURPOSE: Human neutrophil peptides (HNP1-3), small molecular antimicrobial peptides, are expressed within tumors and associated with tumor necrosis and inhibition of angiogenesis. Recent investigations have suggested that HNP1-3 are likely to be involved in the host immune responses to tumors. EXPERIMENTAL DESIGN: We used recombinant pSec-HNP1, which expresses a secretable form of HNP1, to obtain expression of HNP1 in the tumor milieu in immunocompetent mice to explore the possible roles of HNP1 in tumor immunity. The antitumor effects were investigated in established CT26 colon cancer and 4T1 breast cancer models. RESULTS: HNP1-mediated chemotactic and activating effects on immature dendritic cells were detected both in vitro and in vivo. Intratumoral expression of HNP1 resulted in not only significant tumor growth inhibition but also increased CTL infiltration within tumors. Adoptive transfer of splenocytes and a (51)Cr release assay revealed specific cellular immune responses. Furthermore, increased antibodies were also found in sera from pSec-HNP1-treated mice supporting specific humoral immune responses. Increased apoptosis and decreased angiogenesis were also shown in treated tumors. CONCLUSIONS: These findings indicate that HNP1 can exert multiple antitumor effects through different mechanisms; more importantly, HNP1 mediates host immune responses to tumors in situ through the recruitment and subsequent activation of immature dendritic cells and thus shows promising potential in cancer therapy. (Clin Cancer Res 2009;15(22):OF1-11).

• Humoral immunity responses against EGFR-positive tumor cells induced by xenogeneic EGFR expressed in the yeast Pichia pastoris.

  Authors: Fang Fang, Ping Chen, Xian-Cheng Chen, Jiong Li, Yan-Jun Wen, Yu-Quan Wei

  International journal of molecular medicine. 03/2009; 23(2):181-8.

  The breaking of immune tolerance against self epidermal growth factor receptor (EGFR) should be a promising approach for the treatment of those receptor-positive tumors. We have previously shown thatThe breaking of immune tolerance against self epidermal growth factor receptor (EGFR) should be a promising approach for the treatment of those receptor-positive tumors. We have previously shown that human EGFR as a xenoantigen induced a specific antitumor activity against EGFR-positive mouse tumors. Our further studies demonstrated that a recombinant form of extracellular domain of mouse EGFR provoked active cellular immunity responses against EGFR-positive human tumors. In this study, we investigated whether the recombinant murine EGFR expressed in the yeast Pichia pastoris would induce humoral immunity responses against EGFR-positive human tumors. To test this concept, polyclonal immunoglobulin (IgG), which was produced by vaccinating the rabbits with the recombinant mEGFR, was purified from the sera of the rabbits. We evaluated the antitumor activity of the polyclonal IgG in the nude mice bearing A431 tumors. Mice were i.v. treated with the purified IgG at 100 mg/kg 1 day before the mice were inoculated with the tumor cells and then twice per week for 4 weeks. Our results showed that the polyclonal IgG would efficiently inhibit the growth of the solid tumor in vivo. The antitumor effect of the polyclonal IgG may result from the increasing rate of apoptosis and induction of differentiation of the tumor cells in vivo. The present findings may provide insight into treatment of EGFR-positive tumors through induction of the humoral immunity responses based on xenogeneic homologous EGFR.

• Liposomal honokiol inhibits VEGF-D-induced lymphangiogenesis and metastasis in xenograft tumor model.

  Authors: Jing Wen, A-Fu Fu, Li-Juan Chen, Xing-Jiang Xie, Guang-li Yang, Xian-Cheng Chen, Yong-Sheng Wang, Jiong Li, Ping Chen, Ming-Hai Tang, Xi Ming Shao, You Lu, Xia Zhao, Yu-Quan Wei

  International journal of cancer. Journal international du cancer. 01/2009;

  Lymph nodes metastasis of tumor could be a crucial early step in the metastatic process. Induction of tumor lymphangiogenesis by vascular endothelial growth factor-D may play an important role inLymph nodes metastasis of tumor could be a crucial early step in the metastatic process. Induction of tumor lymphangiogenesis by vascular endothelial growth factor-D may play an important role in promoting tumor metastasis to regional lymph nodes and these processes can be inhibited by inactivation of the VEGFR-3 signaling pathway. Honokiol has been reported to possess potent antiangiogenesis and antitumor properties in several cell lines and xenograft tumor models. However, its role in tumor-associated lymphangiogenesis and lymphatic metastasis remains unclear. Here, we established lymph node metastasis models by injecting overexpressing VEGF-D Lewis lung carcinoma cells into C57BL/6 mice to explore the effect of honokiol on tumor-associated lymphangiogenesis and related lymph node metastasis. The underlying mechanisms were systematically investigated in vitro and in vivo. In in vivo study, liposomal honokiol significantly inhibited the tumor-associated lymphangiogenesis and metastasis in Lewis lung carcinoma model. A remarkable delay of tumor growth and prolonged life span were also observed. In in vitro study, honokiol inhibited VEGF-D-induced survival, proliferation and tube-formation of both human umbilical vein endothelial cells (HUVECs) and lymphatic vascular endothelial cells (HLECs). Western blotting analysis showed that liposomal honokiol-inhibited Akt and MAPK phosphorylation in 2 endothelial cells, and downregulated expressions of VEGFR-2 of human vascular endothelial cells and VEGFR-3 of lymphatic endothelial cells. Thus, we identified for the first time that honokiol provided therapeutic benefit not only by direct effects on tumor cells and antiangiogenesis but also by inhibiting lymphangiogenesis and metastasis via the VEGFR-3 pathway. The present findings may be of importance to investigate the molecular mechanisms underlying the spread of cancer via the lymphatics and explore the therapeutical strategy of honokiol on antilymphangiogenesis and antimetastasis. (c) 2008 Wiley-Liss, Inc.

• [Researches on cloning and expression of the gene encoding Schistosoma japonicum tetraspanins extracellular loop 2 and its immunogenicity]

  Authors: Yi-Jie Fu, Li Yang, Kang Liu, Chuang Yuan, Xian-Cheng Chen, Yu-Quan Wei

  Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition. 12/2008; 39(6):890-4.

  OBJECTIVE: To clone and express the gene (Sj-tsp-2) encoding extracellular loop 2 (EC-2) of tetraspanins (TSPs) of Schistosoma japonicum (Chinese strain), and then to study the antigenicity andOBJECTIVE: To clone and express the gene (Sj-tsp-2) encoding extracellular loop 2 (EC-2) of tetraspanins (TSPs) of Schistosoma japonicum (Chinese strain), and then to study the antigenicity and immunogenicity of this protein. METHODS: Synthesized Sj-tsp-2 gene was cloned into prokaryotic expression vector pET32a to generate pET32a-Sj-tsp-2 recombinant plasmid, and transformed into competent E. coli BL21 (DE3). After inducing with IPTG, the expressed fusion protein was purified under nondenaturing conditions. RESULTS: The recombinant was confirmed by sequence analysis. The size of fusion protein and interest peptide was accords with the theoretical value by SDS-PAGE analysis. Additionally, the results of Western Blotting and ELISA demonstrated that the expressed protein had good immunogenicity. More importantly, we confirmed that TSP-2 is mainly located on the surface of S. japonicum. CONCLUSION: The successful expression and purification of recombinant protein Trx-Sj-TSP-2 will be very helpful for the further study of its protection role in animals.

• A promising cancer gene therapy agent based on the matrix protein of vesicular stomatitis virus.

  Authors: Ju-Mei Zhao, Yan-Jun Wen, Qiu Li, Yong-Sheng Wang, Hong-Bo Wu, Jian-Rong Xu, Xian-Cheng Chen, Yang Wu, Ling-Yu Fan, Han-Shuo Yang [......] Xiao-Bo Du, Peng Diao, Jiong Li, Hong-Bing Wu, Bing Kan, Song Lei, Hong-Xin Deng, Yong-Qiu Mao, Xia Zhao, Yu-Quan Wei

  The FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 09/2008;

  The matrix (M) protein of vesicular stomatitis virus (VSV) plays a key role in inducing cell apoptosis during infection. To investigate whether M protein-mediated apoptosis could be used in cancerThe matrix (M) protein of vesicular stomatitis virus (VSV) plays a key role in inducing cell apoptosis during infection. To investigate whether M protein-mediated apoptosis could be used in cancer therapy, its cDNA was amplified and cloned into eukaryotic expression vector pcDNA3.1(+). The recombinant plasmid or the control empty plasmid pcDNA3.1(+) was mixed with cationic liposome and introduced into various tumor cell lines in vitro, including lung cancer cell LLC, A549, colon cancer cell CT26 and fibrosarcoma cell MethA. Our data showed that the M protein induced remarkable apoptosis of cancer cells in vitro compared with controls. Fifty micrograms of plasmid in a complex with 250 microg cationic liposome was injected intratumorally into mice bearing LLC or MethA tumor model every 3 days for 6 times. It was found that the tumors treated with M protein plasmid grew much more slowly, and the survival of the mice was significantly prolonged compared with the mice treated with the control plasmid. In MethA fibrosarcoma, the tumors treated with M protein plasmid were even completely regressed, and the mice acquired longtime protection against the same tumor cell in rechallenge experiments. Both apoptotic cells and CD8(+) T cells were widely distributed in M protein plasmid-treated tumor tissue. Activated cytotoxic T lymphocytes (CTLs) were further detected by means of (51)Cr release assay in the spleen of the treated mice. These results showed that M protein of VSV can act as both apoptosis inducer and immune response initiator, which may account for its extraordinary antitumor effect and warrant its further development in cancer gene therapy.-Zhao, J., Wen, Y., Li, Q., Wang, Y., Wu, H., Xu, J., Chen, X., Wu, Y., Fan, L., Yang, H., Liu, T., Ding, Z., Du, X., Diao, P., Li, J., Wu, H., Kan, B., Lei, S., Deng, H., Mao, Y., Zhao, X., Wei, Y. A promising cancer gene therapy agent based on the matrix protein of vesicular stomatitis virus.

• Long-term stable expression of antisense cDNA of cyclin B1 profoundly inhibits the proliferation of tumor cells and suppresses tumorigenicity in implanted mice.

  Authors: Tao Zhang, Ling Zhang, Ji-Cheng Li, Dong Wei, Yu-Quan Wei, Ru Zhang, Peng Cheng, Xian-Cheng Chen, Huan-Yi Liu, Xiao-Mei Su

  Chinese medical journal. 09/2008; 121(15):1433-8.

  BACKGROUND: Cyclin B1 (CLB1) is necessary for mitotic initiation in mammalian cells and plays important roles in cancer development. Therefore, a potential strategy in cancer therapy is to suppressBACKGROUND: Cyclin B1 (CLB1) is necessary for mitotic initiation in mammalian cells and plays important roles in cancer development. Therefore, a potential strategy in cancer therapy is to suppress the activity of CLB1 by delivering antisense constructs of CLB1 into tumor cells. In previous CLB1 studies, antisense constructs with a short half life were often used and these constructs might not persistently inhibit CLB1. METHODS: We successfully created a recombinant plasmid encoding the full-length antisense cDNA of mouse cyclin B1 (AS-mCLB1) and transfected this construct to the murine Lewis lung carcinoma (LL/2) and CT-26 colon carcinoma (CT-26) cells. We isolated clones of LL/2 and CT-26 transfectants with stable expression of AS-mCLB1. Reverse transcriptional polymerase chain reaction (RT-PCR) and Western blot were applied to detect the expression of the mRNA and protein levels of CLB1. To further test the efficacy of this strategy in vivo, AS-mCLB1-expressing LL/2 and CT-26 transfectants were implanted into mice. RESULTS: We found the expression of the mRNA and protein levels of CLB1 decrease in these transfectants. The inhibition of CLB1 caused prominent G1 arrest, abnormal morphology, retarded cell growth and an increase in apoptosis. In AS-mCLB1-expressing LL/2 and CT-26 transfectants implanted mice, tumorigenicity was effectively suppressed compared with the controls. In addition, the expression of AS-mCLB1 also significantly increases the survival duration of implanted animals. CONCLUSION: AS-mCLB1 is likely to be useful in future cancer therapy, which may be associated with its ability to down-regulate the expression of CLB1 and then induce G1arrest and apoptosis in tumor cells.

• Human alpha-defensin-1 inhibits growth of human lung adenocarcinoma xenograft in nude mice.

  Authors: Ning Xu, Yong-Sheng Wang, Wu-Bin Pan, Bo Xiao, Yan-Jun Wen, Xian-Cheng Chen, Li-Juan Chen, Hong-Xin Deng, Jia You, Bing Kan, A-Fu Fu, Dan Li, Xia Zhao, Yu-Quan Wei

  Molecular cancer therapeutics. 07/2008; 7(6):1588-97.

  Human alpha-defensin-1 (HNP1), a small antimicrobial peptide, shows cytotoxicity to tumor cells in vitro and inhibitory activity for pathologic neovascularization in vivo. Here, we did a gene therapyHuman alpha-defensin-1 (HNP1), a small antimicrobial peptide, shows cytotoxicity to tumor cells in vitro and inhibitory activity for pathologic neovascularization in vivo. Here, we did a gene therapy with a plasmid that expresses a secretable form of HNP1 for assaying its antitumor activity. The expression and secretion of HNP1 were determined by reverse transcription-PCR and ELISA in vitro. We found that expression of HNP1 in A549 tumor cells caused significant growth inhibition. This effect is most likely cell autonomous, as a significant amount of recombinant HNP1 protein was found to be accumulated in the cytoplasm by immunohistochemical staining using an anti-HNP1 antibody and the supernatant containing secreted HNP1 failed to produce any noticeable antitumor activity. Flow cytometry and Hoechst 33258 staining showed that the number of apoptotic cells among the A549 cells expressing recombinant HNP1 proteins was significantly greater than that of the nontransfected control cultures, suggesting that this growth-inhibitory activity was due to an apoptotic mechanism triggered by the intracellular HNP1. The antitumor activity of intracellularly expressed HNP1 was also shown in vivo. Decreased microvessel density and increased lymphocyte infiltration were observed in tumor tissue from HNP1-treated mice through histologic analysis. These results indicate that intracellularly expressed HNP1 induces tumor cell apoptosis, which inhibits tumor growth. The antiangiogenesis effect of HNP1 may contribute to its inhibitory activity in vivo, and HNP1 might involve the host immune response to tumor. These findings provide a rationale for developing HNP1-based gene therapy for cancer.

• Immunity against tumor angiogenesis induced by a fusion vaccine with murine beta-defensin 2 and mFlk-1.

  Authors: Yong-Sheng Wang, Guo-Qing Wang, Yan-Jun Wen, Lian Wang, Xian-Cheng Chen, Ping Chen, Bin Kan, Jiong Li, Canhua Huang, You Lu, Qin Zhou, Ning Xu, Dan Li, Ling-Yu Fan, Tao Yi, Hong-Bo Wu, Yu-Quan Wei

  Clinical cancer research : an official journal of the American Association for Cancer Research. 12/2007; 13(22 Pt 1):6779-87.

  PURPOSE: Previous studies indicated that humoral or cellular immunity against murine vascular endothelial growth factor 2 (mFlk-1) was elicited to inhibit tumor growth. Here we describe a geneticPURPOSE: Previous studies indicated that humoral or cellular immunity against murine vascular endothelial growth factor 2 (mFlk-1) was elicited to inhibit tumor growth. Here we describe a genetic fusion vaccine, pMBD2-mFlk-1, based on the targeting of a modified mFlk-1 to antigen-presenting cells by a murine beta-defensin 2 (MBD2) protein to induce both humoral and cellular immunity against mFlk-1, with the targeting especially focused on immature dendritic cells. EXPERIMENTAL DESIGN: The protective and therapeutic antitumor immunity of the fusion vaccine was investigated in mouse models. Antiangiogenesis effect was detected by immunohistochemical staining and alginate-encapsulate tumor cell assay. The mechanisms of the fusion vaccine were primarily explored by detection of autoantibodies and CTL activity and confirmed by the deletion of immune cell subsets. RESULTS: The fusion vaccine elicited a strong protective and therapeutic antitumor immunity through antiangiogenesis in mouse models, and this worked through stimulation of an antigen-specific CD8+ T-cell response as well as a specific B-cell response against mFlk-1. The findings were confirmed by depletion of immune cell subsets and in knockout mice. CONCLUSION: Our study showed that a fusion vaccine based on self immune peptide (MBD2) and self antigen (mFlk-1) induced autoimmunity against endothelial cells, resulting in inhibition of tumor growth, and could be further exploited in clinical applications of cancer immunotherapy.

• Prophylaxis against carcinogenesis in three kinds of unestablished tumor models via IL12-gene-engineered MSCs.

  Authors: Xian-Cheng Chen, Rui Wang, Xia Zhao, Yu-Quan Wei, Min Hu, Yang-sheng Wang, Xiao-wei Zhang, Ru Zhang, Lin Zhang, Bin Yao [......] Ting-Ting Zeng, Jin-Liang Yang, Ling Tian, Bing Kan, Xiao-juan Lin, Song Lei, Hong-Xin Deng, Yan-Jun Wen, Yong-Qiu Mao, Jiong Li

  Carcinogenesis. 12/2006; 27(12):2434-41.

  Mesenchymal stem cells (MSCs) were adenovirally engineered to secrete interleukin-12 (AdIL-12-MSCs) and evaluated for their anticarcinogenesis efficacy against three kinds of unestablished tumorMesenchymal stem cells (MSCs) were adenovirally engineered to secrete interleukin-12 (AdIL-12-MSCs) and evaluated for their anticarcinogenesis efficacy against three kinds of unestablished tumor models including B16 melanoma, LLC Lewis lung cancer and HCC hepatoma. Injection of AdIL-12-MSCs into protected mice before tumor inoculation prevented all of 12 mice in B16 preventive groups, 10 out of 12 in LLC lung cancer model and 11 out of 12 mice in HCC hepatoma model from developing tumors, whereas the control groups pre-receiving PBS were validated for 100% carcinogenesis; the tumor formation rates in free-AdIL-12 and vacant MSC groups were unveiled between approximately 83 and 100% even with plentiful angiogenesis and newborn lymphatic vessels, as well as distant metastases. As a novel approach, AdIL-12-MSC has revealed expected preventive effects on carcinogenesis (P<0.01) with low-toxic, broad-spectrum and long-range superiorities. In conclusion, our data indicate that AdIL-12-MSC possess the potential for tropism to preclinical tumor lesions and deprives surviving or hibernating tumor cells, which have escaped from conventional treatments, of revival and recurrence.

• [Construction of pORF-mIG and activity evaluation of MIG in vitro]

  Authors: Ru Zhang, Ling Tian, Fei Xiao, Yan-Jun Wen, Jiong Li, Jian-Mei Hou, Ling Zhang, Gang Li, Bing Yao, Xian-Cheng Chen, Kai Mel

  Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition. 08/2006; 37(4):502-5.

  OBJECTIVE: To establish a transformant of monokine induced by interferon-gamma (MIG) with the eukaryotic expression vector for further investigating the efficacy of its use in antitumor gene therapy.OBJECTIVE: To establish a transformant of monokine induced by interferon-gamma (MIG) with the eukaryotic expression vector for further investigating the efficacy of its use in antitumor gene therapy. METHODS: The MIG full-length cDNA was amplified from pBLAST-MIG and was cloned into the eukaryote expression vector pORF-mcs, and the resulted recombinant plasmid was named pORF-MIG. The recombinant pORF-MIG was determined with restriction enzyme and sequencing, and then it was transfected into COS-7 cells by Lipfectamin. Expression of the transformant was detected by immunoblot assay, and the bioactivity was assessed by chemotaxis assay. RESULTS: The restriction analysis and the sequence determination confirmed that the recombinant pORF-MIG contained the MIG full-length cDNA. And the transformants of pORF-MIG expressed the MIG protein which could apparently attract the activated lymphocytes. CONCLUSION: The recombinant pORF-MIG was constructed successfully, and this recombinant eukaryotic expression vector could be used in additional studies on the biological effect of MIG and its use in anti-tumor gene therapy.