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  Poster Display session (Friday) (ID 65)

  • Event: ELCC 2018
  • Type: Poster Display session
  • Track:
  • Presentations: 1
  • Now Available
  • Moderators:
  • Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1

  • 25241

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    11P - Glycolysis enzyme screenings identify non-glycolytic function of aldolase A that interacts and alters F-actin dynamics to promote lung cancer metastasis (Now Available) (ID 168)

    12:30 - 12:30  |  Presenting Author(s): Y. Chang
    • Abstract
    • Slides

    Background:
    In recent years, cancer metastasis remains a serious issue for drug development and target therapy. Although the metabolic reprogramming including glycolysis appears to promote cancer metastasis, the molecular mechanism by which this occurs remains unclear.
    
    Methods:
    From high throughput screening of glycolytic enzymes, we investigated aldolase A (ALDOA) as the most significant enzyme promoting cell metastasis in vitro and in vivo. Furthermore, we recruited the enzyme inhibitors and enzyme-dead constructs to compromised function of aldolase A.
    
    Results:
    We established a His-tagged ALDOA construct model and found ALDOA directed protein-protein interaction (PPI) with g-actin and the status correlated with malignant cancer cells, whereas in normal cell it did not. Meta-analysis of intergraded RNA and protein levels suggested ALDOA could be a prognostic marker in several cancer types. Moreover, compared with non-tumor tissues increased levels of ALDOA and g-actin are commonly detected in malignancies and strongly predict a worse prognosis in cancer patients. Therefore, we designed a specific peptide to block the interaction between ALDOA and g-actin to decrease the metastatic ability of cancer cells in vitro and prolong survival rate in vivo.
    
    Conclusions:
    These findings suggest a new therapeutic strategy for targeting the cancer-associated PPI between ALDOA and g-actin to combat metastatic cancers.
    
    Clinical trial identification:
    
    
    Legal entity responsible for the study:
    Genomics Research Center, Academia Sinica, Taiwan
    
    Funding:
    Has not received any funding
    
    Disclosure:
    All authors have declared no conflicts of interest.
    
    

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