Virtual Library

 x 
My Library Virtual Library FAQ

Start Your Search

Y. Zhang



Author of

  • +

    P1.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 233)

    • Event: WCLC 2015
    • Type: Poster
    • Track: Biology, Pathology, and Molecular Testing
    • Presentations: 2
    • +

      P1.04-046 - MFN2 Regulates Lung Adenocarcinoma Cell Proliferation and Invasion (ID 2231)

      09:30 - 09:30  |  Author(s): Y. Zhang

      • Abstract

      Background:
      Mitofusin-2 gene (MFN2) encodes a mitochondrial protein which is critical for mitochondrial fusion process. MFN2 was initially identified as a hypertension-associated gene and implicated in the pathogenesis of multiple cancer types. However, roles and underlying mechanisms of MFN2 in lung adenocarcinoma development remain to be determined.

      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 effects of MFN2 knockdown on cell proliferation, cell cycle process, cell migration and invasion was investigated in A549 cells. Then MFN2-knockdown induced gene expression changes in A549 cells was analyzed by microarray assay and then functional pathway enrichment analysis was performed to identify critical pathways involved in MFN2-mediated lung adenocarcinoma development. The expression changes of downstream factors were further determined in A549 cells by western blot.

      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 (Fig. 1A, B). Furthermore, MFN2 knockdown inhibited cell proliferation (Fig. 1C), induced cell cycle arrest (Fig. 1E) and blocked invasion behavior (Fig. 1D) in A549 lung adenocarcinoma cells. Microarray analysis revealed that a lot of genes were deregulated in A549 cells with MFN2 knockdown (Fig. 1F). Then functional pathway enrichment revealed six pathways were enriched in deregulated genes including Cell cycle, DNA replication, ECM-receptor interaction, Focal adhesion, MAPK signaling pathway and Chemokine signaling pathway (Fig. 1G). Furthermore, the downregulation of RAP1A and upregulation of RALB and ITGA2 identified in MFN2-knockdown cells by microarray analysis were confirmed by western blot (Fig. 1H).Figure 1



      Conclusion:
      Our results confirmed the involvement of MFN2 in the pathogenesis of lung adenocarcinoma and revealed that MFN2 was critical for cell proliferation and invasion in lung adenocarcinoma cell line A549. Furthermore, microarray analysis identified multiple pathways deregulated in MFN2-knockdown cells, providing valuable insights about the mechanisms underlying MFN2-associated lung adenocarcinoma development.

    • +

      P1.04-090 - Roles of MLF1IP in the Proliferation of Lung Adenocarcinoma Cells (ID 2234)

      09:30 - 09:30  |  Author(s): Y. Zhang

      • Abstract

      Background:
      MLF1IP was initially identified as a MLF1 interacting protein, which encodes a centromere protein essential for cell cycle and mitosis. It has been reported that MLF1IP depletion impaired the interaction between centromere and microtubules, finally inducing defects in cell mitosis. However, the involvement of MLF1IP in lung adenocarcinoma development and related mechanisms remain to be elucidated.

      Methods:
      MLF1IP expression at mRNA level in 15 pair lung adenocarcinoma/adjacent normal lung samples was examined with real-time PCR assay. Then the expression of MLF1IP in human lung adenocarcinoma cells A549 was inhibited with lentiviral-mediated shRNA strategy. Effects of MLF1IP knockdown on cell proliferation was analyzed by Cellomics cell counting method and MTT assay. Then the impact of MLF1IP knockdown on colony formation, cell cycle process and cell survival was determined in A549 cells by colonogenesis assay, PI staining and Annexin V-APC staining respectively.

      Results:
      MLF1IP expression was significantly increased in lung adenocarcinomas as compared to adjacent normal lung tissues (fold change=2.50, P<0.05), with higher MLF1IP expression observed in 66.7% (10/15) samples while lower expression observed in only 20% (3/15) samples (Fig. 1A). Furthermore, MLF1IP knockdown impaired cell proliferation (Fig. 1B, C), inhibited colony formation ability (Fig. 1D), induced cell cycle arrest (Fig. 1E) and promoted cell apoptosis (Fig. 1F) in A549 lung adenocarcinoma cells.Figure 1



      Conclusion:
      Our study showed that MLF1IP expression is correlated with lung adenocarcinoma development and MLF1IP expression is critical for cell proliferation and survival in lung adenocarcinoma cell line A549. MLF1IP represents a novel potential target for lung adenocarcinoma therapy.

  • +

    P2.06 - Poster Session/ Screening and Early Detection (ID 219)

    • Event: WCLC 2015
    • Type: Poster
    • Track: Screening and Early Detection
    • Presentations: 1
    • +

      P2.06-002 - Preliminary Results of Early Stage Lung Cancer Detection Using Low-Dose Computed Tomographic Screening (ID 609)

      09:30 - 09:30  |  Author(s): Y. Zhang

      • Abstract

      Background:
      The overall 5 years survival for lung cancer patients is approximately 16%, a survival advantage is noted for early stage lung cancer, with 5-year survivals up to 65%. However, only 10% patients are diagnosed when the primary tumor is resectable. Our trial was conducted to improving the early stage lung cancer detection rate using low-dose CT.

      Methods:
      Eligible participants enrolled in our trial were local residents in 6 communities located in Xuhui District, Shanghai, China, aged from 45 to 70 years and with either of the following risk factors: 1) history of cigarette smoking ≥ 20 pack-years, and, if former smokers, had quit within the previous 15 years; 2) malignant tumors history in immediate family members; 3) personal cancer history; 4) professional exposure to carcinogens; 5) long term exposure to second-hand smoke; 6) long term exposure to cooking oil fumes. From November 2013 to November 2014, the high risk residents received free chest low-dose CT (LDCT) scans at Shanghai Jiao Tong University Affiliated Shanghai Chest Hospital. The findings of CT scan were identified by three experts. The shadows on the lungs were grouped accordingly. If imaging was highly suggestive of malignancy, the expert group would have further discussion. The residents would be assigned to undergo biopsy or surgical resection directly.

      Results:
      Up to January 2015, 2933 participants were received LDCT screening. According to the inclusion criteria, 2892 persons at high risk for lung cancer were included in our trail, and 41cases were finally excluded. Of the 2892 aged 45 -70 years old cases, the median age was 61years old. Of the included participants, 1151 cases were male, and 1741 cases were female. Pulmonary small nodules were found in 742 cases; small nodules detection rate was 25.66% (742/2892). 69 cases were suspected of lung cancer. Accounting for pulmonary small nodules was 9.30% (69/742), and was 2.39% (69/2892) of the total number of screening high risk population. 23 cases underwent surgery, with 22 lung cancer (10 males and 12 females) and 1 hamartoma, representing a positive lung cancer detection rate with low-dose CT screening of 0.76% (22/2892). 21 of the 22 cases resected lung cancers were stage I (95.45%) and 1 was stage II (4.55%), with 21 adenocarcinomas (95.45%) and 1 squamous lung cancer (4.55%).

      Conclusion:
      The application of low-dose CT screening prompted an increase detection rate of early stage lung cancers (stage I and II) in the high risk population.