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Y. Chang



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    Poster Display session (Friday) (ID 65)

    • Event: ELCC 2018
    • Type: Poster Display session
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 4/13/2018, 12:30 - 13:00, Hall 1
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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 (ID 168)

      12:30 - 13:00  |  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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