Pingqing Tan

Central South University, Changsha, Hunan, China

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Publications (4)6.26 Total impact

  • Article: [Synergistic interactions of TRAIL and paclitaxel on the nasopharyngeal carcinoma cell lines in vitro].
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    ABSTRACT: To investigate the synergistic cytotoxicity of TRAIL and paclitaxel on nasopharyngeal cell lines CNE-1 and CNE-2. CCK-8 assays the growth inhibition rate of CNE-1 and CNE-2 which was treated with TRAIL or paclitaxel or conbination of both. Flow cytometry tests the apoptosis rate of CNE-1 and CNE-2 which was treated with TRAIL or paclitaxel or conbination of each other. In certain range of time and concentration,TRAIL and paclitaxel inhibited the growth of the cell lines of CNE-1 and CNE-2 in a time-dose dependent manner (P < 0.05). The rate of growth inhibition and apoptosis in TRAIL and paclitaxel combinative group was more significant than that in the TRAIL and paclitaxel singular group (P < 0.05). TRAIL and paclitaxel had a synergistic killing effect on NPC cell lines and showed better effection than singular group, which provides a novel and prospective strategy for NPC chemotherapy.
    Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 04/2012; 26(7):319-22.
  • Article: Inhibiting ERp29 expression enhances radiosensitivity in human nasopharyngeal carcinoma cell lines.
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    ABSTRACT: ERp29 is an endoplasmic reticulum (ER) stress-inducible protein. It was found that ERp29 was highly expressed in several cancers and associated with resistance to oxidative and radiation stress, which may serve as a novel target for nasopharyngeal carcinoma (NPC) anticancer approach. In this study, we used immunohistochemistry to detect ERp29 expression in radioresistant and radiosensitive NPC tissues. As a result, ERp29 was up-regulated in radioresistant NPC tissues compared to radiosensitive NPC tissues. We also found that ERp29 knockdown attenuated radioresistance of NPC CNE-1 cells and ERp29 overexpression enhanced radioresistance of NPC CNE-2 cells. When exposed to radiation, ERp29 knockdown CNE-1 cells increased radiation-induced cell apoptosis and ERp29 overexpression CNE-2 cells reduced radiation-induced cell apoptosis. Further, we demonstrated that ERp29 up-regulated the expression of Hsp27. In conclusion, our study supports ERp29 could potentiate resistance to radiation in NPC cells, targeting of ERp29 is a rational strategy in treating radioresistant NPC.
    Medical Oncology 04/2011; 29(2):721-8. · 2.14 Impact Factor
  • Article: [The expression and correlation of HMGB1 and VEGF protein in laryngeal squamous cell carcinoma].
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    ABSTRACT: To investigate the expression and biological significance of HMGB1 and VEGF protein in tissue specimens of laryngeal squamous cell carcinoma (LSCC), and further study the correlation between HMGB1 and VEGF protein. The expression of HMGB1 and VEGF protein was evaluated by immunohistochemical staining in 69 cases of LSCC specimens and 15 cases of adjacent epithelial tissue samples, and futher correlated with clinicopathologic parameters. The positive rates of HMGB1 and VEGF in LSCC tissues were significantly higher than those in adjacent non-cancerous mucosa (P < 0.01), and the expression of these two marks was closely correlated with clinical stage (P < 0.05) and metastasis (P < 0.05) in LSCC. While the expression of HMGB1 and VEGF had no significant correlations with age, sex, histological differentiation and tumor site (P > 0. 05). There was a positive correlation between the expression of HMGB1 and VEGF (P < 0.05). The Kaplan-Meier survival analysis showed that patients with strong expression of HMGB1 or VEGF had poorer overall survival compared with that in patients with relative low HMGB1 or VEGF expression (P < 0.05). Multivariate COX regression analysis revealed that both lymph node metastasis and HMGB1 expression were independent prognostic factors for patients with LSCC. This study demonstrated that HMGB1 and VEGF protein overexpression were closely associated with clinical stage, metastasis and poorer prognosis in patients with LSCC. Increased expression of these two proteins in LSCC suggested that HMGB1 and VEGF might play a critical role in the initiation and progression of LSCC.
    Lin chuang er bi yan hou ke za zhi = Journal of clinical otorhinolaryngology 03/2011; 25(6):265-9.
  • Article: Elevated expression of HMGB1 in squamous-cell carcinoma of the head and neck and its clinical significance.
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    ABSTRACT: HMGB1 overexpression has been reported in a variety of human cancers. However, the role of HMGB1 in squamous-cell carcinoma of the head and neck (SCCHN) remains unclear. The aim of the present investigation was to analyse HMGB1 protein expression in both SCCHN tissue and cell levels and to assess its prognostic significance in SCCHN. HMGB1 protein expression in 103 primary SCCHN tissue specimens was analysed by immunohistochemistry and correlated with clinicopathological parameters and patient outcome. Additionally, HMGB1 protein expression was evaluated in cell level by Western blotting. By Western blotting analysis, all the 5 SCCHN cell lines overexpressed HMGB1 protein, whereas the non-transformed immortalised cell line NP-69 had relatively weak HMGB1 protein expression. Immunohistochemical staining revealed that HMGB1 protein was detected in 91 (91/103, 88.3%) primary tumour samples, but only in 7 (7/16, 43.75%) adjacent non-carcinoma samples (p<0.001); moreover, HMGB1 overexpression was significantly associated with T classification (p=0.001), clinical stage (p<0.001), recurrence (p<0.001) and lymph node metastasis (p<0.001). Survival analysis demonstrated that high HMGB1 expression was significantly associated with shorter disease-free and overall survival (both p<0.001), especially in late patients with SCCHN. When HMGB1 expression and lymph node status were combined, patients with HMGB1 overexpression/lymph node (+) had both poorer disease-free and overall survival than others (both p<0.001). Multivariate analysis further demonstrated that HMGB1 was an independent prognostic factor for patients with SCCHN. HMGB1 protein may contribute to the malignant progression of SCCHN, and present as a novel prognostic marker and a potential therapeutic target for patients with SCCHN.
    European journal of cancer (Oxford, England: 1990) 11/2010; 46(16):3007-15. · 4.12 Impact Factor