Research Information System
American Society for Biochemistry and Molecular Biology (ASBMB) Annual Meeting, Texas, United States Of America, 23 March 2024, pp.1, (Summary Text)
Abnormal expression/activation of Notch is associated with cancer development (Guo et al.,
2011). Notch activity is specifically increased in tumor endothelium and in various tumor types.
Since the Notch signaling pathway can mediate communication between various cell types in
the tumor microenvironment, interactions between tumor cells and endothelial cells can promote
angiogenesis (Rehman AO 2006). The levels of IL-1α/-β ligands, which are components of the
IL-1 system, are increased in breast cancer. In studies conducted in breast cancer cells, leptin
increased the mRNA and protein levels of all components of the IL-1 system (Gonzalez-Perez
RR 2010).Leptin is a cytokine secreted by adipocytes and cancer cells that promotes
angiogenesis. Increased leptin signaling is associated with the expression of proteins and is
implicated in cancer progression and tumor angiogenesis (Gonzalez-Perez et al., 2013). An
interaction between Notch, leptin and IL-1 signaling (NILCO) affects the expression of
pro-angiogenic molecules, leading to cell proliferation and migration of breast cancer cells (Guo
and Gonzalez-Perez, 2011). Leptin signaling has been shown to regulate VEGF/VEGFR-2,
Notch and its targets in breast cancer (Guo and Gonzalez-Perez, 2011). In addition, leptin may
contribute to angiogenesis, migration and proliferation through its induction (Ruben Rene
Gonzalez-Perez 2013).In this study, we aimed to show the interactions of NILCO signaling
pathways with each other as a result of the inhibition of each of them separately and their
MMP-related contributions on angiogenesis, migration and proliferation. For this purpose, we
tried to explain the mechanisms of action on angiogenic molecules, cell proliferation and
migration by inhibiting NILCO-related genes in the human colorectal cancer (CRC) cell line
HCT-15.