Aurelio Minuti

@università degli studi di messina



           

https://researchid.co/aureliominuti

RESEARCH, TEACHING, or OTHER INTERESTS

Biochemistry, Genetics and Molecular Biology, Cell Biology, Endocrinology, Cancer Research

3

Scopus Publications

Scopus Publications

  • Antimicrobial Susceptibility of Staphylococcus aureus Strains and Effect of Phloretin on Biofilm Formation
    Giuseppina Mandalari, Aurelio Minuti, Erminia La Camera, Davide Barreca, Orazio Romeo, and Antonia Nostro
    Springer Science and Business Media LLC

  • Endocan Knockdown Down-Regulates the Expression of Angiogenesis-Associated Genes in Il-1ß Activated Chondrocytes
    Michele Scuruchi, Federica Aliquò, Angela Avenoso, Giuseppe Mandraffino, Giovanna Vermiglio, Aurelio Minuti, Salvatore Campo, Giuseppe Maurizio Campo, and Angela D’Ascola
    MDPI AG
    Endocan is a small soluble proteoglycan (PG) known to be involved in inflammation and angiogenesis. Increased endocan expression was found in the synovia of arthritic patients and chondrocytes stimulated with IL-1ß. Considering these findings, we aimed to investigate the effects of endocan knockdown on the modulation of pro-angiogenic molecules expression in a model of IL-1ß-induced inflammation in human articular chondrocytes. Endocan, VEGF-A, MMP-9, MMP-13, and VEGFR-2 expression was measured in both normal and endocan knockdown chondrocytes stimulated with IL-1ß. VEGFR-2 and NF-kB activation were also measured. Results have shown that endocan, VEGF-A, VEGFR-2, MMP-9, and MMP-13 were significantly up-regulated during IL-1ß-induced inflammation; interestingly, the expression of such pro-angiogenic molecules and NF-kB activation were significantly reduced by endocan knockdown. These data support the hypothesis that endocan released by activated chondrocytes may be involved in the mechanisms that stimulate cell migration and invasion, as well as angiogenesis, in the pannus of arthritic joints.

  • Endocan Promotes Pro-Tumorigenic Signaling in Lung Cancer Cells: Modulation of Cell Proliferation, Migration and lncRNAs H19 and HULC Expression
    Federica Aliquò, Aurelio Minuti, Angela Avenoso, Giuseppe Mandraffino, Giuseppe Maurizio Campo, Salvatore Campo, Angela D‘Ascola, and Michele Scuruchi
    MDPI AG
    Endocan is a circulating proteoglycan secreted by several cell lines and identified as a potential biomarker of inflammation and angiogenesis. Endocan-increased expression has been found in a broad spectrum of human tumors, including lung cancer, and is associated with a poor prognosis. To elucidate the possible mechanism, this study aimed to investigate the role of endocan in non-small-cell lung carcinoma (NSCLC) using an in vitro model of cultured cells. Endocan expression was knocked down by using a specific small interfering RNA. The effects of endocan knockdown have been evaluated on VEGF-A, VEGFR-2, HIF-1α, the long non-coding RNAs H19 and HULC expression, and AKT and ERK 1/2 degree of activation. Cell migration and proliferation have been studied as well. VEGF-A, VEGFR-2, HIF-1α, and the long non-coding RNAs H19 and HULC expression were significantly affected by endocan knockdown. These effects correlated with a reduction of cell migration and proliferation and of AKT and ERK 1/2 activation. Our findings suggest that endocan promotes a more aggressive cancer cell phenotype in NSCLC.