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C. Shi



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    Poster Session (ID 8)

    • Event: ACLC 2018
    • Type: Poster Session
    • Track:
    • Presentations: 1
    • Moderators:
    • Coordinates: 11/07/2018, 00:00 - 00:00, Poster Hall
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      P037 - QSOX1/2 Regulates (ID 197)

      00:00 - 00:00  |  Author(s): C. Shi

      • Abstract

      Background:
      Elevated plasma concentration of Lipoprotein [a] (Lp(a)) is considered to be one of the important risk factors for coronary heart disease (CHD) and calcific aortic valve stenosis (CAVS), In recent years, the concentration of Lp(a) has been found to be elevated in plasma in some cancer patients without cardiovascular disease, However, the involvement of Lp(a) in the development of oncology and its regulatory mechanism is not fully understood. Previous studies have suggested that QSOX (Quiescin/sulfhydryl oxidase) may be involved in the synthesis of Lp(a) in vitro, but whether the process has an abnormal activation in the tumour is unclear.


      Method:
      Serum samples from 75 patients with lung, stomach, colorectal and ovarian cancer without cardiovascular disease and 50 normal subjects were collected at random. Lp(a) concentration was measured by Immunoturbidimetric assay (ITA). The expression levels of QSOX1/2 in 32 patients with lung, gastric, colorectal and ovarian cancer were measured by Enzyme-linked immunosorbent assay (ELISA) and westernblot. The difference expression of QSOX1/2 between tumor and para-cancerous tissues in TCGA-Pancancer database was analyzed by bioinformatics method. The difference gene analysis and pathway analysis of QSOX1/2 high and low expression groups were performed by Bayesian method, and the correlation between QSOX1/2 expression level and survival and clinical stage was further analyzed. In vitro, the ability to synthesize Lp(a) of HepG2 cells after QSOX1/2 deletion was verified by Immunoturbidimetric assay (ITA), and cell proliferation was analyzed by EdU and flow cytometry.


      Results:
      We found that serum Lp(a) concentrations in 27.5% of patients in the study cohort were higher than the mean value in the normal medical cohort. Serum Lp(a) concentrations in cancer patients were positively correlated with QSOX1/2 serum concentrations (R=0.34?P<0.005). In the TCGA-Pancancer database, the expression level of QSOX1/2 in tumor tissues were higher than that in para-cancerous tissues, and the over expression of QSOX1/2 may be related to abnormal regulation of tumor cell cycle. In vitro, experiments showed that the expression of QSOX1/2 regulated the extracellular synthesis ability of Lp(a). Silencing QSOX1/2 genes significantly inhibited the proliferation of tumor cells.


      Conclusion:
      The abnormal expression of QSOX1/2-Lp(a) can be used as a potential bio-marker for the poor prognosis of cancers. And targeted QSOX1/2 treatment may inhibit tumor growth with this molecular subtype.