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L. Jiang



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    Poster Display Session (ID 63)

    • Event: ELCC 2017
    • Type: Poster Display Session
    • Track:
    • Presentations: 3
    • Moderators:
    • Coordinates: 5/07/2017, 12:30 - 13:00, Hall 1
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      15P - PLGF regulates crosstalk between non-small cell lung cancer cells and tumor-associated macrophages in cancer vascularization and growth (ID 253)

      12:30 - 13:00  |  Author(s): L. Jiang

      • Abstract

      Background:
      The growth and invasion of non-small cell lung cancer (NSCLC) require assistance of tumor-associated vascularization, the underlying molecular mechanisms of which remain eluted. Recently, we reported that placental growth factor (PLGF) was expressed by NSCLC cells, and promoted the metastasis of NSCLC cells. Here, we showed that NSCLC cells produced and secreted PLGF to signal to tumor-associated macrophages (TAM) through the surface expression of the receptor for PLGF, Flt-1, on macrophages.

      Methods:
      Ten week-old male NOD/SCID mice were used for transplantation of 10[7] AAV-transduced/labeled A549 cells by tail vein injection. Bones from 12-week-old male C57BL/6 mice were flushed with macrophage culture media. Isolated bone-marrow-derived macrophages (10[5]) were co-cultured either with equal number of A549 cells (10[5]) with/without of 10µmol/l SB431542, or with/without recombinant PLGF (100ng), or with/without of 10 µg/l sFlt-1. Two days after co-culture, the changes in A549 cell number were determined with an MTT assay, and the macrophage subtypes were determined by flow cytometry.

      Results:
      In a transwell co-culture system, PLGF secreted by NSCLC cells triggered macrophage polarization to a TAM subtype that promote growth of NSCLC cells. Moreover, polarized TAM seemed to secrete transforming growth factor β 1 (TGFβ1) to enhance the growth of endothelial cells in a HUVEC assay.

      Conclusions:
      Thus, our studies suggest that the cross-talk between TAM and NSCLC cells via PLGF/Flt-1 and TGFβ receptor signaling may promote the growth and vascularization of NSCLC.

      Clinical trial identification:


      Legal entity responsible for the study:
      Shanghai Chest Hospital

      Funding:
      This work was supported by the National Natural Science foundation of China (81402378).

      Disclosure:
      All authors have declared no conflicts of interest.

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      168P - Clinical and prognostic characteristics of primary pulmonary non-Hodgkin’s lymphoma: A retrospective analysis of 38 cases in a Chinese population (ID 194)

      12:30 - 13:00  |  Author(s): L. Jiang

      • Abstract

      Background:
      Primary pulmonary non-Hodgkin’s lymphoma(NHL) is very rare, and although the prognosis is favorable, clinical features, beneficial diagnostic procedures, prognostic factors and optimal management have not been clearly defined.

      Methods:
      In this study, thirty-eight cases of primary pulmonary NHL treated in Shanghai Chest Hospital during a 10-year period were retrospectively reviewed, and clinicopathological features and prognosis were analyzed.

      Results:
      There were twenty-eight patients with mucosa-associated lymphoid tissue (MALT) lymphoma, three with diffuse large B-cell lymphoma, one with peripheral T-cell lymphoma, one with mantle cell lymphoma and five with unclassified B-cell lymphoma. The cohort consisted of 21 male and 17 female patients with a median age of 57.5 years. At presentation, 36.8% of patients were asymptomatic, and unilateral tumors occurred more frequently than bilateral and predominantly in the right lung. Thirty-three patients underwent surgical resection single or combination chemotherapy, and five patients received combination chemotherapy alone. Overall survival(OS) was significantly longer in patients with MALT lymphoma than that of non-MALT lymphoma (129.9 vs. 71.5 months, P = 0.019 by log-rank test). Patients who had received surgical resection had a better OS (126 vs. 65.4 months, P = 0.036 by log-rank test). Additionally, multivariate analysis showed that elevated serum lactate dehydrogenase (LDH) level was independently associated with a poor OS (P = 0.048).

      Conclusions:
      Primary pulmonary NHL has atypical clinical manifestations and non-specific imaging changes. Surgical resection is vital in clarifying the diagnosis and obtaining a favorable prognosis. Serum LDH level was an independent prognostic factor.

      Clinical trial identification:


      Legal entity responsible for the study:
      Shanghai Chest Hospital

      Funding:
      Shanghai Chest Hospital

      Disclosure:
      All authors have declared no conflicts of interest.

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      9P - Knockdown of MFN2 gene expression inhibits lung adenocarcinoma cell proliferation (ID 254)

      12:30 - 13:00  |  Author(s): L. Jiang

      • Abstract

      Background:
      Mitofusin-2(MFN2) was initially identified as a hyperplasia suppressor in hyper-proliferative vascular smooth muscle cells of hypertensive rat arteries, which has also been implicated in various cancers. There exists a controversy in whether it is an oncogene or exerting anti-proliferative effect on tumor cells. Our previous cell cycle analysis and MTT assay showed that cell proliferation was inhibited in MFN2 deficient A549 human lung adenocarcinoma cells. MFN2-knockdown induced gene expression changes in A549 cells was analyzed by microarray assay and then functional pathway enrichment analysis revealed that six pathways were enriched in deregulated genes including Cell cycle, DNA replication, ECM-receptor interaction, Focal adhesion, MAPK signaling pathway and Chemokine signaling pathway, as we previously reported.

      Methods:
      MFN2 expression at protein level was examined in 30 pair lung adenocarcinoma/adjacent normal lung samples with immunohistochemistry staining. Then MFN2 knockdown was performed in human lung adenocarcinoma cells A549 with lentiviral-mediated shRNA strategy. The expression changes of downstream factors were determined in A549 cells by western blot. Furthermore, tumor models in nude mice were generated and tumor formation and progression in these mice were analysed.

      Results:
      As compared to adjacent normal lung tissues, MFN2 expression was significantly higher in lung adenocarcinoma tissues with positive MFN2 signals in 90% (27/30) lung adenocarcinoma tissues and only in 26.7% (8/30) adjacent normal tissues. The downregulation of RAP1A and upregulation of RALB and ITGA2 identified in MFN2-knockdown cells by microarray analysis were confirmed by western blot. In vivo, tumor models in nude mice were generated. Tumor formation and progression in nude mice suggested that MFN2 knockdown reduced tumorigenesis of A549 cells.

      Conclusions:
      The current study confirmed the anti-proliferative effect of MFN2 deficiency and its risk in lung adenocarcinoma.

      Clinical trial identification:


      Legal entity responsible for the study:
      Shanghai Chest Hospital

      Funding:
      This work was supported by the National Natural Science foundation of China (81572249 and 81201839).

      Disclosure:
      All authors have declared no conflicts of interest.