Junke Fu

Tianjin Medical University, T’ien-ching-shih, Tianjin Shi, China

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Publications (10)3.74 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: It has been confirmed that nm23-H1 gene is one of the tumor metastasis suppressor genes. Up to now, the exact mechanism of nm23-H1 gene is uncertian. The aim of this study is to compare the biological behavior changes among three human high-metastatic large cell lung cancer cell lines which transfected and untransfected nm23-H1 gene, and to study the mechanism of nm23-H1 gene supressing the metastasis. Boyden Chamber and MTT method were used to detect the rates of invasion and proliferation among different human pulmonary carcinoma cells of transfected and untransfected nm23-H1 gene; meanwhile The three lung cancer cell lines were treated with PKC inhibitor Calphostin C, and the above measurements were also performed. The ability of invasion and proliferation of L9981 and L9981-PLXSN human high-metastatic large cell lung cancer cells,which lack of nm23-H1gene, was higher than that of L9981-nm23-H1 human high-metastatic large cell line, which transfected with nm23-H1gene (P <0.001). There was no difference beteween L9981 and L9981-PLXSN cell lines (P >0.05). After treated with PKC inhibitor Calphstin C,the invasion and proliferation ability of three lung cancer cell lines were obviously go down (P <0.001), however, the invasion and proliferation ability of L9981-nm23-H1 lung cancer cell line was still lower than those of L9981 and L9981-PLXSN lung cancer cell lines (P <0.001), and there was also no significant difference between two later cell lines (P >0.05). Our data suggest that nm23-H1 gene can significantly inhibit the cell proliferation and invasion in L9981 lung cancer line. The effect of nm23-H1 might be correlated with downregulation of PKC signal transduction in human high-metastatic large cell lung cancer cell line.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 06/2008; 11(3):349-53. DOI:10.3779/j.issn.1009-3419.2008.03.035
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    ABSTRACT: Protein Kinase C (PKC) is one of the key kinases in the cell signal transduction passway. There are more reports about it's ability on cell proliferation, but fewer on invasion and metastasis in the past; and it's mechanisms are unclear. The aim of this study is to analyze the variation of intracellular distribution and translocation of the protein kinase C alpha among human high-metastatic large cell lung cancer cell line with different metastasis potential,in order to investigate the correlation between the lung carcinoma invasion and metastasis and the PKC isoforms. Using Western blot and laser scanning confocal microscope (LSCM) method. The distribution of PKC alpha in cytosol and plasma membrane and translocation were detected among different metastatic potential human pulmonary carcinoma cells L9981, L9981-pLXSN and L9981-nm23-H1 before and after treatment with PKC inhibitor Calphostin C, by Western blot and LSCM. PKC alpha in L9981 and L9981- pLXSN was mainly expressed on membrane, which was remarkably higher than those in L9981-nm23-H1 cell line (P =0.001); while expression of PKC alpha in cytoslol in L9981 and L9981-pLXSN cell lines, was lower than those in L9981-nm23-H1 cell line (P <0.001). The expression of PKC alpha in cytosol in L9981-nm23-H1 cell line was remarkably higher than those in L9981 and L9981-pLXSN cell lines (P <0.001), while expression of PKC alpha in plasma membrane in L9981-nm23-H1 cell line, was significantly lower than those in L9981 and L9981- pLXSN cell lines (P =0.001). PKC alpha is mainly located in nucleus and perinucleus in L9981 and L9981-pLXSN cells, which was in active status, In L9981-nm23-H1 cell line, PKC alpha is mainly located in soluble cytosolic section, which was in inactive status. After treated with PKC inhibitor Calphostin C, the expression of PKC alpha in membrane in L9981, L9981-pLXSN and L9981-nm23-H1 was downregulated, and PKC alpha were observed mainly located in cytosolic site in all the three cell lines, which was mainly in inactive status. The study suggests that PKC isoforms is closely correlated with human lung cancer invasion and metastasis.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 06/2008; 11(3):363-7. DOI:10.3779/j.issn.1009-3419.2008.03.034
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    ABSTRACT: Up to now, locally advanced non-small cell lung cancer simutaneously involving carina, heart and great vessels is still regarded as contraindication for surgical treatment. However, the prognosis is very poor in these patients treated with chemotherapy and/or chemoradiotherapy. The aim of this study is to summarize the clinical experiences of carinoplasty combined with heart and great vessel plasty in the treatment of 84 patients with locally advanced non-small cell lung cancer involving carina, heart and great vessels or both in our hospital. From March, 1988 to December, 2004, carinal resection and reconstruction combined with heart, great vessel plasty was performed in 84 patients with locally advanced non-small cell lung cancer involving carina, heart and great vessels simutaneously. The operative procedures in this series included as follows: (1) Right upper sleeve lobectomy combined with carinal resection and reconstruction, and right pulmonary artery sleeve angioplasty in 9 patients; (2) Right sleeve pneumonectomy combined with partial resection and reconstruction of left atrium, and superior vena cava resection and Gortex grafts in 3 cases; (3) Left upper sleeve lobectomy combined with carinoplasty, left pulmonary artery sleeve angioplasty and partial resection and reconstruction of left atrium in 3 cases; (4) Right upper sleeve lobectomy combined with carinoplasty, right pulmonary artery sleeve angioplasty and partial resection and reconstruction of left atrium in 10 cases; (5) Left upper sleeve lobectomy combined with carinoplasty and left pulmonary artery angioplasty in 9 cases; (6) Left upper sleeve lobectomy combined with carinoplasty, left pulmonary artery sleeve angioplasty and resection of the aorta arch sheath in 6 cases; (7) Right upper-middle sleeve lobectomy combined with carinoplasty and right pulmonary artery sleeve angioplasty in 3 cases; (8) Left upper sleeve lobectomy combined with carinoplasty, left pulmonary artery angioplasty, resection of the aorta arch sheath and partial resection and reconstruction of left artium in 8 cases; (9) Right upper sleeve lobectomy combined with carinoplasty, right pulmonary artery angioplasty and partial resection and reconstruction of left atrium in 4 cases; (10) Left sleeve pneumonectomy combined with partial resection and reconstruction of left atrium in 3 cases; (11) Right upper-middle sleeve lobectomy combined with carinoplasty, right pulmonary artery angioplasty and superior vena cava resection and reconstruction with Gortex grafts in 23 casese; (12) Right sleeve pneumonectomy combined with partial resection and reconstruction of left atrium in 1 case; (13) Right upper-middle sleeve lobectomy combined with carinoplasty, right pulmonary artery angioplasty and partial resection and reconstruction of left atrium in 1 case; (14) Right upper-middle sleeve lobectomy combined with carinoplasty, right pulmonary artery angioplasty and right inferior pulmonary vein sleeve resection and reconstruction in 1 case. There were two operative death in this series. The operative mordality was 2.38%. A total of 32 patients had operative complications. The incidence of operative complications was 38.10%. The 1-, 3-, 5-and 10-year survival rate was 81.34%, 59.47%, 31.73% and 24.06% respectively. (1) It is feasible in technique that carinal resection and reconstruction combined with heart, great vessel plasty in the treatment of locally advanced non-small cell lung cancer involving carina, heart and great vessels simutaneously; (2) Multiple modality therapy based on carinal resection and reconstruction combined with heart and great vessel plasty can remarkably increase the survival rate, and improve the prognosis and quality of life in patients with locally advanced non-small cell lung cancer involving carina, heart and great vessels.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 02/2006; 9(1):2-8. DOI:10.3779/j.issn.1009-3419.2006.01.02
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    ABSTRACT: To explore the effects of transfection of nm23-H1 gene on expression of β-catenin and phospho-β-catenin in human high-metastatic large cell lung cancer line L9981, and to provide evidence to elucidate the molecular mechanism of nm23-H1 mediated tumor metastatic suppression. To determine whether nm23-H1 contributes to cytoplasm and nuclear β-catenin and phospho-β-catenin expression, the expression level of β-catenin and phospho-β-catenin in cytoplasm and nucleus was detected in human high-metastatic large cell lung carcinoma cell lines including primary cell line L9981 with nm23-H1 gene deletion, L9981-nm23-H1 transfected with nm23-H1 gene, and L9981-pLXSN transfected with vector by Western blot. (1)β-catenin expression in L9981-nm23-H1 cytoplasm (IOD) (3 649±118) was significantly higher than that in L9981 (1 401±31) and L9981-pLXSN (1 350±55) cell lines (P < 0.001);(2)There was no statistical diffe-rence of the β-catenin expression in nucleus among L9981-nm23-H1 (2 945±68), L9981 (2 604±23) and L9981-pLXSN (2 652±53) cell lines (P > 0.05);(3)Phospho-β-cetenin expression of cytoplasm in L9981-nm23-H1 cell line (3 123±102) was significantly lower than that in L9981 (4 362±131) and L9981-pLXSN ( 4 500 ±117) cell lines (P < 0.001);(4)Phospho-β-catenin expression of nucleus in L9981-nm23-H1 (5 136±112) was significantly higher than that in L9981 (2 666±116) and L9981-pLXSN (2 661±66) cell lines (P < 0.001);(5)There was no statistical difference of β-catenin or phospho-β-catenin expression in cytoplasm and nucleus between L9981 and L9981-pLXSN cell lines (P > 0.05). (1)nm23-H1 gene transfection can remarkably upregulates the expression of cytoplasm β-catenin in human high-metastatic large cell lung cancer cell line L9981, but do not induce the nucleus accumulation of β-catenin; (2)Transfection of nm23-H1 gene can significantly upregulate the expression of phospho-β-catenin in nucleus and remarkably downregulate the expression of phospho-β-catenin in cytoplasm of L9981; (3)Regulation of the expression of the key modecule, β-catenin, in Wnt signal pathway might be the important melecular mechanisms which nm23-H1 gene controls "Lung Cancer Metastatic Suppresive Cascade" and reverves cancer metastasis in L9981.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 12/2004; 7(6):471-4. DOI:10.3779/j.issn.1009-3419.2004.06.02
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    ABSTRACT: To explore the possibility of targeting blockage of Wnt signal transduction pathway of nm23-H1 gene transfection in human high-metastatic large cell lung cancer cell line L9981, and to provide evidence to elucidate the signal conductive mechanism of nm23-H1 mediated tumor metastasis suppression. The expression of GSK-3β and β-catenin of Wnt signal pathway was detected in cytoplasm and nucleus in L9981 cell line with nm23-H1 deletion, L9981-pLXSN cell line transfected with vector and L9981-nm23-H1 cell line transfected with nm23-H1 gene by Western blot. (1)GSK-3β expression in L9981-nm23-H1 cytoplasm (6 341±541) was significantly higher than those in L9981 (3 736±298) and L9981-pLXSN (3 613±383) cell lines ( P < 0.001); (2)GSK-3β expression in L9981-nm23-H1 nucleus (4 356±490) was significantly higher than those in L9981 (657±57) and L9981-pLXSN (705±75) cell lines ( P < 0.001); (3)β-catenin expression in L9981-nm23-H1 cytoplasm (3 649±118) was significantly higher than those in L9981 (1 401±31) and L9981-pLXSN (1 350±55) cell lines ( P < 0.001); (4)No statistical difference of the β-catenin expression in nucleus was observed among L9981-nm23-H1 (2 945±68), L9981 (2 604±23) and L9981-pLXSN (2 652±53)( P > 0.05); (5)No significant difference of GSK-3β or β-catenin expression in cytoplasm and nucleus was observed between L9981 and L9981-pLXSN ( P > 0.05). (1)nm23-H1 gene can remarkably upregulate the expression of GSK-3β in cytoplasm and nucleus, and β-catenin expression in cytoplasm in L9981-nm23-H1 cell, but can not induce the nucleus accumulation of β-catenin. (2)Regulation of GSK-3β and β-catenin expression, and targeting blockage of Wnt signaling pathway may be one of molecular mechanisms that nm23-H1 contributes to play a vital role in the "Lung Cancer Metastasis Suppressive Cascade".
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 08/2004; 7(4):294-7. DOI:10.3779/j.issn.1009-3419.2004.04.06
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    ABSTRACT: To investigate the influence of tumor metastasis suppressor gene nm23-H1 on the activity of glycogen synthase kinase 3β (GSK-3β) in human high-metastasis large cell lung cancer cell line L9981. The levels of GSK-3β expression in cytoplasm and nucleus were determined with anti- GSK-3β antibody in human high-metastasis large cell lung cancer cell line L9981 (cell line with nm23-H1 gene deletion), L9981-nm23-H1 (cell line with nm23-H1 transfected) and L9981-pLXSN (cell line with vector transfected) by Western blot method. The activity of GSK-3β among those three cell lines was detected by immunoprecipitation and analysed by a radioactive isotope scintillation counter before and after treating with 20 mmol/L LiCl. (1) The expression indensity of GSK-3β of cytoplasm and nucleus was (6 341±541) and (4 356±490) IOD in L9981-nm23-H1, (3 613±383) and (705±75) IOD in L9981-pLXSN, and (3 736±298) and (675±57) IOD in L9981, respectively. A high significance in GSK-3β expressive indensity of both cytoplasm and nucleus existed among L9981-nm23-H1, L9981-pLXSN and L9981 (P < 0.01); Multiple comparison: A highly significant difference was observed when L9981-nm23-H1 was compared with L9981-pLXSN or L9981 (P < 0.01), but no significant difference was observed between L9981-pLXSN and L9981 (P > 0.05). (2) The GSK-3β activity of cytoplasm and nucleus was (28 955±2 509) and (9 247±924) CPM in L9981-nm23-H1, (11 241±1 495) and (1 492±176) CPM in L9981-pLXSN, and (12 505±1 469) and (1 763±125) CPM in L9981, respectively. A highly significant difference in GSK-3β activity of both cytoplasm and nucleus existed among L9981-nm23-H1, L9981-pLXSN and L9981 (P < 0.01); Multiple comparison: the GSK-3β activity in L9981-nm23-H1 was significantly higher than that in L9981-pLXSN and L9981 (P < 0.01), but no significant difference was observed between the L9981-pLXSN and L9981 (P > 0.05). (3) After treatment with 20 mmol/L LiCl, the expressive indensity of GSK-3β of cytoplasm and nucleus was (4 718±549) and (3 823±350) IOD in L9981-nm23-H1, (2 030±155) and (217±15) IOD in L9981-pLXSN, and (2 164±151) and (224±19) IOD in L9981, respectively. No significant difference in GSK-3β expressive indensity existed between before and after treatment with LiCl in L9981-nm23-H1 (P > 0.05). However, the GSK-3β expressive indensity in cytoplasm and nucleus before treatment was remarkably higher than those after treatment in both L9981-pLXSN and L9981 (P < 0.05). (4) After treatment with 20 mmol/L LiCl, the GSK-3β activity in cytoplasm and nucleus was (11 099±1 112) and (3 748±215) CPM in L9981-nm23-H1, (4 447±430) and (1067±159) CPM in L9981, and (4 435±427) and (909±156) CPM in L9981-pLXSN, respectively. The GSK-3β activity both in cytoplasm and nucleus after treatment with LiCl was remarkably lower than that before treatment in L9981-nm23-H1, L9981-pLXSN and L9981 (P < 0.01 or P < 0.05). (1) Transfection of nm23-H1 gene can significantly up-regulate the expression level and activity of GSK-3β in human high-metastasis large cell lung cancer cell line L9981; (2) LiCl can remarkably suppress the upregulation effects of nm23-H1 gene on GSK-3β activity in L9981 cell line; (3) The effects of nm23-H1 gene on suppressing the signal transduction of Wnt pathway might be carried out through upregulating GSK-3β expression and activity in human high-metastasis large cell lung cancer cell line L9981.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2004; 7(2):81-5. DOI:10.3779/j.issn.1009-3419.2004.02.01
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    ABSTRACT: To explore the effects of nm23-H1 gene transfection and forskolin on PKA activity in human high-metastasis large cell lung cancer cell line L9981. Three cell lines, primary human large cell lung cancer cell line (L9981), vector transfection cell line (L9981-pLXSN) and nm23-H1 gene transfection cell line (L9981-nm23-H1-pLXSN), were treated with PKA activator forskolin. The PKA activity at different time points after treatment with forskolin was detected in the three lung cancer cell lines by radioimmunological method with SignaTECT cAMP-dependent PKA assay system. (1) Before forskolin treatment, the activity of PKA of L9981-nm23-H1-pLXSN was remarkably higher than those of L9981 and L9981-pLXSN (P < 0.01), but no significant difference in the PKA activity was observed between L9981 and L9981-pLXSN (P > 0.05). (2)The PKA activity was remarkably increased in all the three lung cancer cell lines after treatment with different concentration of forskolin (P < 0.01), and up to the highest level at the concentration of 100 μmol/L. It showed a dose-dependent relationship between the PKA activity and forskolin concentration; (3) The PKA activity in all the three cell lines was elevated to the highest level at 30 minutes after treatment with forskolin of 100 μmol/L, and it showed a time-dependent relationship between the PKA activity and action time of forskolin. (1)Transfection of nm23-H1 gene can up-regulate the PKA activity of human high-metastasis large cell lung cancer cell line L9981, and its function as a tumor metastasis suppressor gene may be related to its effects on regulation of PKA signal transduction pathways; (2)Forskolin can remarkably up-regulate the PKA activity of L9981 cell line, and the elevation of PKA activity has a time-dependent and dose-dependent relation to forskolin.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2004; 7(2):91-4. DOI:10.3779/j.issn.1009-3419.2004.02.03
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    ABSTRACT: To explore the influences of nm23-H1 gene transfection and protein kinase C (PKC) inhibitor Calphostin C on PKC signal transduction pathway in human high-metastasis large cell lung cancer cell line L9981, and to evaluate the effects of nm23-H1 gene on translocation and activation in subcellular region. The translocation of PKC in subcellular region was observed in L9981 before and after nm23-H1 gene transfection and Calphostin C treatment by Laser scanning confocal microscope (LSCM) method. PKC-α and PKC-βII were found to locate in different subcellular site in L9981 before and after nm23-H1 gene transfection. PKC-α and PKC-βII mainly located in nucleus and perinucleus in L9981 and L9981-pLXSN cell lines, which were in active status. PKC-α and PKC-βII mainly located in soluble cytosolic fraction in L9981-nm23-H1 cell line and were inactive status. PKC-α and PKC-βII mainly located in cytosolic fraction and were in inactive status in all the three cell lines after treatment with Calphostin C. The results suggest that nm23-H1 gene might make PKC to translocate from nucleus and perinucleus to soluble cytosolic fraction in L9981 cell line. PKC inhibitor, Calphostin C, can also make PKC to translocate from nucleus and perinucleus to soluble cytosolic fraction in L9981, L9981-pLXSN cell lines. Both transfection of nm23-H1 gene and treatment with Calphostin C can suppress the PKC signal transduction in L9981 cell line.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 04/2004; 7(2):86-90. DOI:10.3779/j.issn.1009-3419.2004.02.02
  • Lung Cancer 08/2003; 41. DOI:10.1016/S0169-5002(03)92371-3 · 3.74 Impact Factor
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    ABSTRACT: To summarize the clinical results of bronchoplastic procedures and pulmonary artery reconstruction or combined with other resection and plasty of heart, great vessels in the treatment of 304 patients with locally advanced lung cancer. From February, 1983 to December, 2001, double sleeve resection and reconstruction of bronchus and pulmonary artery, or combined with other resection of heart, great vessels were carried out in 304 patients with locally advanced lung cancer. The operations included double sleeve left upper lobectomy in 199 cases; double sleeve right upper lobectomy in 21 cases; double sleeve right upper middle lobectomy in 14 cases; double sleeve left upper lobectomy combined with resection of left atrium in 8 cases; double sleeve right upper lobectomy combined with superior vena cava (SVC) resection and reconstruction with Gortex graft in 29 cases; double sleeve right upper middle lobectomy combined with SVC resection and reconstruction in 21 cases; double sleeve right upper middle lobectomy, carinal and SVC resection and reconstruction in 11 cases; left pneumonectomy combined right main pulmonary artery and pulmonary artery trunk resection and reconstruction with Gortex graft in 1 case. There were 3 operative deaths. The operative mortality was 1% in this series. Sixty four patients had operative complications. The operative complication rate was 21.05% (64/304). The 1-, 3-, 5- and 10 year survival rates were 81.75%, 60.14%, 37.21% and 24.39% respectively. Double sleeve lobectomy or comblined with other resection and reconstruction of heart, great vessels can significantly improve the prognosis and increase the curative rate and long term survival in patients with locally advanced lung cancer.
    Zhongguo fei ai za zhi = Chinese journal of lung cancer 12/2002; 5(6):403-7. DOI:10.3779/j.issn.1009-3419.2002.06.02

Publication Stats

2 Citations
3.74 Total Impact Points

Institutions

  • 2008
    • Tianjin Medical University
      T’ien-ching-shih, Tianjin Shi, China
    • Henan Provincial People’s Hospital
      Cheng, Henan Sheng, China