Gongyan Chen

Publications (2)0.42 Total impact

• Article: [Establishment of animal model of a human lung adenocarcinoma drug-resistant
cell line Anip973/NVB and investigation on mechanism of drug resistance].

  Meng Wang, Xuan Hong, Qinwen Sun, Ruilin Li, Zhaoyang Yang, Gongyan Chen
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  ABSTRACT: Multidrug resistance (MDR) is the main cause of chemotherapeutic failure in lung cancer, and vinorelbine (NVB) is one of the most efficient drugs that threaten non-small cell lung cancer (NSCLC). The current study aims to establish tumor xenografts and investigate the molecular mechanisms involved in the resistance of NVB in lung adenocarcinoma. Nude mice were implanted with Anip973 and Anip973/NVB, and tumor-bearing mice were divided into the Anip973 treatment, Anip973 control, Anip973/NVB treatment, and Anip973/NVB control groups, respectively. The current study observes tumor growth, draws growth curves, and calculates inhibitory rates. The morphological changes in cell tumor were observed through the immunohistochemical method using an electron microscope to detect the expressions of MRP3 and Bcl-2 and to investigate the molecular mechanisms of Anip973/NVB cells. The tumor inhibitory rates of the Anip973 and Anip973/NVB cells treated with NVB were 60.00% and 4.65%, respectively, compared with the control group. The growth inhibition in the Anip973/NVB cell transplantation tumor had no significant difference. Apoptosis was observed using TEM when the Anip973 transplantation tumor was treated with NVB. On the other hand, no apoptosis was found in the Anip973/NVB transplantation tumor using TEM. Immunohistochemical staining (SP) shows the positive expressions of Bcl-2 and MRP3 proteins in Anip973/NVB transplantation tumor, which were observed to be higher than those in the Anip973 transplantation tumor. The overexpression of Bcl-2 and MRP3 might be one of the major mechanisms of the MDR of Anip973/NVB.
  Zhongguo fei ai za zhi = Chinese journal of lung cancer 03/2012; 15(3):146-51.
• Article: STAT5a-targeting miRNA enhances chemosensitivity to cisplatin and 5-fluorouracil in human colorectal cancer cells.

  Xuan Hong, Gongyan Chen, Meng Wang, Changjie Lou, Yinling Mao, Zhiwei Li, Yanqiao Zhang
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  ABSTRACT: Signal transducers and activators of transcription 5 (STAT5) has been shown to be involved in a variety of cellular processes, including survival, proliferation, invasion, angiogenesis and immune evasion and is frequently overexpressed in human solid tumors and blood malignancies. The aim of this study was to investigate the role of STAT5a in colorectal cancer (CRC) progression. We inhibited the expression of STAT5a using lentivirus-mediated artificial microRNA (miRNA) interference in vitro and investigated the viability of CRC cells by CCK-8 assay. We observed the cell viability after treatment with cisplatin (CDDP) or 5-fluorouracil (5-Fu) by CCK-8 assay, and the apoptosis induced by chemotherapy using flow cytometric analysis and Annexin V RFP staining assay. We inhibited the mRNA expression by 54% and the protein expression by 60% of STAT5 by RNA interference targeting STAT5a. Cell viability assays showed that inhibition of STAT5a did not affect the viability of SW1116 cells. However, we found that inhibition of STAT5a restored the sensitivity of SW1116 cells to CDDP and 5-Fu. In additional experiments, we found that inhibition of STAT5a significantly promoted CRC cell apoptosis by CDDP and 5-Fu. In the present study, we found that inhibition of STAT5a promotes apoptosis of CRC cells induced by chemotherapy drugs, such as CDDP or 5-Fu. These results suggest that inhibition of STAT5a may serve as a potential new target for CRC treatment.
  Molecular Medicine Reports 02/2012; 5(5):1215-9. · 0.42 Impact Factor