Yunfeng Li

Publications of Yunfeng Li

• BH3-based Fusion Artificial Peptide Induces Apoptosis and Targets Human Colon Cancer.

  Authors: Yongjun Liu, Yunfeng Li, Haijuan Wang, Jing Yu, Hongwei Lin, Dongkui Xu, Yang Wang, Ailing Liang, Xiao Liang, Xueyan Zhang, Ming Fu, Haili Qian, Chen Lin

  Molecular therapy : the journal of the American Society of Gene Therapy. 05/2009;

  Dysregulation of apoptosis is a pilot event before cancer development and plays important roles for cancer to develop resistance to chemical therapeutics. So exploring strategies to recovery theDysregulation of apoptosis is a pilot event before cancer development and plays important roles for cancer to develop resistance to chemical therapeutics. So exploring strategies to recovery the apoptosis balance is a charming and long-endeavored aim in the attempts to conquer cancers. The present study shows an exciting potency of a fusion peptide to inhibit and target to cancer cells, which is composed of BH3 (Bcl-2 Homology 3) effector domain from PUMA (p53 upregulated modulator of apoptosis) and targeting domain of trans-activator of transcription (TAT) and DV3. The in vitro results demonstrated cancer growth inhibition by the fusion peptide in colon cancer cells, as well as in lung adenocarcinoma cell line and breast carcinoma cell line of human origin. But the viability of HEK293, a noncancerous cell line, was not affected, indicating the cancer specificity of the fusion peptide. Apoptosis activation was induced by the peptide through the mitochondria pathway. In vivo studies displayed its tumor inhibiting ability by intratumoral injection. When the fusion peptide was administered systematically by tail vein, the peptide targeted the established tumors in nude mice. No other organs were significantly involved. The fusion peptide is an artificially designed molecule worthy of further evaluation and development.Molecular Therapy (2009); doi:10.1038/mt.2009.43.

• Adenoviral-mediated gene transfer of Gadd45a results in suppression by inducing apoptosis and cell cycle arrest in pancreatic cancer cell.

  Authors: Yunfeng Li, Haili Qian, Xiao Li, Haijuan Wang, Jing Yu, Yongjun Liu, Xueyan Zhang, Xiao Liang, Ming Fu, Qimin Zhan, Chen Lin

  The journal of gene medicine. 11/2008;

  BACKGROUND: The extremely poor prognosis of patients with pancreatic ductal adenocarcinoma indicates the need for novel therapeutic approaches. The growth arrest and DNA damage-inducible (Gadd) geneBACKGROUND: The extremely poor prognosis of patients with pancreatic ductal adenocarcinoma indicates the need for novel therapeutic approaches. The growth arrest and DNA damage-inducible (Gadd) gene Gadd45a is a member of a group of genes that are induced by DNA damaging agents and growth arrest signals. METHODS: We evaluated the biological activity of Gadd45a in pancreatic ductal adenocarcinoma cancer-derived cell lines and assessed the efficacy of a combined treatment with adenoviral-mediated expression of Gadd45a (Ad-G45a) and anticancer drug (Etoposide, cisplatin, 5-fluorouracil, respectively) for the PANC1 cell line. RESULTS: Gadd45a is variously expressed in cell lines derived from pancreatic ductal adenocarcinoma cancer and adenoviral-mediated expression of Gadd45a (Ad-G45a) in these cells results in apoptosis via caspase activation and cell-cycle arrest in the G2/M phase. Gadd45a significantly increased the chemosensitivity of PANC1, which may be due to abundant apoptosis induction and cell cycle arrest. By combinational treatment of Ad-G45a infection and chemotherapeutics, Gadd45a expression was elevated to a higher extent in cancer cells with wild-type p53 than in that with knocked-out p53 status, indicating a higher chemosensitivity to cancer chemotherapy. CONCLUSIONS: Gadd45a may be a promising candidate for use in cancer gene therapy in combination with chemotherapeutic agents. Copyright (c) 2008 John Wiley & Sons, Ltd.

• RNA interference of metastasis-associated gene 1 inhibits metastasis of B16F10 melanoma cells in a C57BL/6 mouse model.

  Authors: Haili Qian, Jing Yu, Yunfeng Li, Haijuan Wang, Chongwen Song, Xueyan Zhang, Xiao Liang, Ming Fu, Chen Lin

  Biology of the cell / under the auspices of the European Cell Biology Organization. 11/2007; 99(10):573-81.

  BACKGROUND INFORMATION: MTA1 (metastasis-associated gene 1) has been reported to be overexpressed in cancers with high potential to metastasize. Studies of the molecular mechanisms revealed that MTA1BACKGROUND INFORMATION: MTA1 (metastasis-associated gene 1) has been reported to be overexpressed in cancers with high potential to metastasize. Studies of the molecular mechanisms revealed that MTA1 plays an important role in the process of metastasis of many types of cancer. However, the role of MTA1 in melanoma development is unclear. RESULTS: We have investigated the therapeutic value of MTA1 in the B16F10 melanoma cell line with the C57BL/6 mouse model. Studies in vitro showed that MTA1 promoted the metastatic ability of B16F10 cancer cells. MTA1 down-regulation by RNA interference greatly reversed the malignant phenotypes of cancer cells. Immunohistochemical staining of MTA1 in human melanoma samples confirmed the up-regulation of MTA1 in the process of carcinogenesis. Studies in vivo confirmed down-regulation of MTA1 suppressed the growth and experimental metastasis of B16F10 melanoma cells. CONCLUSIONS: MTA1 plays an important role in melanoma development and metastasis. It has a promising potential as a target for in cancer gene therapy or chemotherapy.

• Arsenic trioxide (As2O3) reduces the invasive and metastatic properties of cervical cancer cells in vitro and in vivo.

  Authors: Jing Yu, Haili Qian, Yunfeng Li, Yang Wang, Xueyan Zhang, Xiao Liang, Ming Fu, Chen Lin

  Gynecologic oncology. 09/2007; 106(2):400-6.

  OBJECTIVES: Arsenic trioxide (As(2)O(3)) was found to induce apoptosis in certain types of cancer cells including acute promyelocytic leukemia, and recently in solid tumors. We have previouslyOBJECTIVES: Arsenic trioxide (As(2)O(3)) was found to induce apoptosis in certain types of cancer cells including acute promyelocytic leukemia, and recently in solid tumors. We have previously demonstrated that As(2)O(3) has a therapeutic effect on cervical cancer by apoptosis promotion in vitro and in vivo. Here we further our study on the role of arsenic trioxide in regulating invasive activity of cervical cancer cells in vitro and in vivo. METHODS: The effects of As(2)O(3) on human cervical cancer cell lines (HeLa, SiHa, Caski) adhesion, migration and invasion were observed by means of cell adhesion test, cell migration test and cell invasion test. The effects of As(2)O(3) on p-IkappaB, MMP-2, E-cadherin, caveolin-1 and beta-catenin protein expressions of tumor cells were determined by Western blot. In addition, the effects of As(2)O(3) on NF-kappaB activity of tumor cells were analyzed by immunoblot in whole lysates, cytosol and nucleus, respectively. In animal experiments, cervical cancer cells TC-1 were injected into tail veins of C57BL/6 mice and then the mice were treated by intraperitoneal injection of different doses As(2)O(3). Lung weights and the foci on the surface of lungs were measured. RESULTS: As(2)O(3) inhibited attachment of tumor cells to Fibronectin and Matrigel, reduced cell motility and inhibited tumor invasion potential. As(2)O(3) treatment also resulted in a positive regulation of caveolin-1, upregulation of E-cadherin and decreased activity of beta-catenin, NF-kappaB and NF-kappaB-regulated gene MMP-2. In animal experiments, lung weights in PBS group (0.31+/-0.07 g) were significantly elevated compared with those in As(2)O(3)-treated groups (0.21+/-0.03 g and 0.17+/-0.03 g) also As(2)O(3) reduced number of metastatic lesions of lungs (15.4+/-3.5 vs. 8.3+/-2.0 and 6.3+/-2.3) in a dose-dependent manner. CONCLUSIONS: This study is the first to report the effectiveness of As(2)O(3) as an inhibitor of cervical cancer invasion both in vitro and in vivo, suggesting a potential clinical application of As(2)O(3) in cervical cancer therapies combining apoptosis induction and metastasis inhibition.

• RNA interference against metastasis-associated gene 1 inhibited metastasis of B16F10 melanoma cell in C57BL/6 model.

  Authors: Haili Qian, Jing Yu, Yunfeng Li, Haijuan Wang, Chongwen Song, Xueyan Zhang, Xiao Liang, Ming Fu, Chen Lin

  Biology of the cell / under the auspices of the European Cell Biology Organization. 06/2007;

  Background information. The metastasis-associated gene 1 (MTA1) has been reported to be overexpressed in cancers with high potential to metastasis. Studies on molecular mechanisms revealed thatBackground information. The metastasis-associated gene 1 (MTA1) has been reported to be overexpressed in cancers with high potential to metastasis. Studies on molecular mechanisms revealed that metastasis-associated gene 1 plays an important role in the process of metastasis of many cancer types. But the role of metastasis-associated gene 1 in melanoma development is unclear. Results. Here we investigated the therapeutic value of metastasis-associated gene 1 in B16F10 cell with C57BL-6 model. Biological studies in vitro showed that metastasis-associated gene 1 promoted the metastatic ability of B16F10 cancer cells. metastasis-associated gene 1 down-regulation by RNA interference (RNAi) greatly reversed the malignant phenotypes of cancer cells. Immunohistochemical staining of metastasis-associated gene 1 in human melanoma samples confirmed the up-regulation of metastasis-associated gene 1 in the process of carcinogenesis. In vivo studies confirmed down-regulation of metastasis-associated gene 1 suppressed the growth and experimental metastasis of B16F10 melanoma cells. Conclusions. Metastasis-associated gene 1 play an important role in melanoma development and metastasis. It bears a promising potential in the application targeting metastasis-associated gene 1 in cancer gene therapy or chemotherapy.

• Therapeutic effect of arsenic trioxide (As2O3) on cervical cancer in vitro and in vivo through apoptosis induction.

  Authors: Jing Yu, Haili Qian, Yunfeng Li, Yang Wang, Xueyan Zhang, Xiao Liang, Ming Fu, Chen Lin

  Cancer biology & therapy. 05/2007; 6(4):580-6.

  Arsenic trioxide (As2O3) induces apoptosis in certain types of cancer cells. But the detailed mechanisms of As2O3 efficacy are not completely known. Here we demonstrate that As2O3 has a therapeuticArsenic trioxide (As2O3) induces apoptosis in certain types of cancer cells. But the detailed mechanisms of As2O3 efficacy are not completely known. Here we demonstrate that As2O3 has a therapeutic effect on cervical cancer in vitro and in vivo. We investigated the As2O3-induced apoptosis in various cervical cancer cells. The apoptosis was triggered by mitochondrial pathway and associated with dissociation of Bcl-2 from Bax and VDAC, then the release of cytochrome c from Bax and VDAC channel, resulting in the activation of caspase-9 and caspase-3. The overexpression of Bcl-2 counteracted the As2O3-mediated apoptosis. The As2O3 treatment also resulted in an increased M phase cell cycle distribution by inducing microtubule polymerization. Two independent death-signaling pathways in cervical cancer cells were activated, one dominated by JNK/p38/GADD45 and one by p53 signals. Further investigation involving assessment of As2O3 on tumor cell growth in mice indicated that As203 also inhibited in vivo tumor growth. As2O3 as an inhibitor of cervical cancer proliferation both in vitro and in vivo suggests a potential clinical application in cervical cancer therapies.