Author of

• 14642

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  P2.07 - Poster Session/ Small Cell Lung Cancer (ID 222)

  • Event: WCLC 2015
  • Type: Poster
  • Track: Small Cell Lung Cancer
  • Presentations: 1
  • Moderators:
  • Coordinates: 9/08/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)

  • 14643

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    P2.07-001 - CK2α Is Highly Expressed and Could Represent a Suitable Therapeutic Target in Small Cell Lung Cancer (ID 2525)

    09:30 - 09:30  |  Author(s): Z. Zhao
    • Abstract

    Background:
    Protein kinase CK2 has long been associated with increased cell growth and proliferation in both normal and malignant cells. CK2α (a catalytic subunit) is highly expressed and pivotal for survival and proliferation in multiple malignancies; however, whether CK2α functions in small cell lung cancer (SCLC) malignant behavior and whether it is feasible to be used as a therapeutic target have not been evaluated.
    
    Methods:
    The expression levels of CK2α were analyzed in SCLC tissue microarray and cell line (NCI-H446) by immunohistochemistry and immunofluorescence. After knocking down the CK 2α level by specific siRNA sequence, biological consequences on proliferation, migration, invasion and apoptosis were evaluated.
    
    Results:
    CK2α was detected in 66.7% of cases with a trend towards a stronger CK2α immunostain in SCLC tissues compared to normal lung tissues. CK2α silencing had potent suppressive effects on SCLC proliferation, migration and invasion, resulted in abrogation of tumor-cell pseudopod formation, however, did not lead to cell arrest and apoptosis. Western-blot analysis confirmed elevated PML/Bcl-2 protein levels as well as reduced E-Cadherin protein level in the CK2α-silenced SCLC cells.

    Patient Characteristics	No. of Cases	%
    Gender (F/M)	9/31	22.5/77.5
    Stage
    Ⅰ	10	25
    Ⅱ	21	52.5
    Ⅲ	9	22.5
    Tumor
    T1/T2	36	90
    T3/T4	4	10
    N0	12	30
    N1/N2	28	70
    Normal Lung Tissue	10

    Figure 1
    
    
    
    Conclusion:
    The results suggest that CK2α negative regulation of the protein levels of tumor suppressor PML/Bcl-2 and activation of the E-Cadherin pathway could be involved in SCLC malignant behavior. Depleting CK2α level may serve as a promising therapeutic strategy for human SCLC.