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Dual effects of C3G in hepatocarcinoma tumor growth and progression

AuthorsSequera, Celia; Arechederra, María; Baquero, Cristina; Palao, Nerea; Guerrero Arroyo, María del Carmen ; Porras, Almudena
Issue Date2017
CitationFEBS3+ (2017)
XL SEBBM Congress (2017)
AbstractC3G is a guanine nucleotide exchange factor for Rap1 and R-Ras. It is essential for embryonic development and regulates several cellular functions such as cytoskeletal remodeling, differentiation and cell death. However, its role in cancer is controversial acting either as a tumor promoter or suppressor. Using different hepatocarcinoma (HCC) cell models with a more epithelial or mesenchymal like phenotype (Hep3B and HLE), we found that C3G knock-down increased invasion and migration through induction of an epithelial-mesenchymal transition (EMT) process. Accordingly, C3G knock-down cells showed higher levels of mesenchymal markers and EMT transcription factors. We have also evaluated the role of C3G in tumorigenesis in HCC cells. In anchorage-dependent assays C3G knock-down led to a reduced number of foci and the cells within a focus were more disperse. This is in agreement with its lower adhesion. In contrast, anchorage independent assays revealed that C3G silencing in Hep3B cells increased the number and size of foci. However, each individual focus was composed of less and scattered cells. We also found that C3G knock-down decreased cell death. Moreover, our preliminary studies showed that C3G down-regulation favors the induction of a stem cell like phenotype in Hep3B cells. Thus, C3G silenced cells form more spheres and increase the expression of some stemness markers. In contrast, in vivo tumor growth in nude mice was reduced in Hep3B cells subjected to C3G knock-down. We are currently analyzing cell death, proliferation, infiltrated fi broblasts, immune cells and the presence of vessels within the tumors. In addition, disseminated cancer cells in blood, lungs and bone marrow are under investigation as a way to evaluate their metastatic capacity in vivo. Altogether, our data support a dual function of C3G in HCC. On one side, C3G acts as a tumor promoter by enhancing adhesion, anchorage-dependent growth and in vivo tumor growth. On the other hand, C3G inhibits migration, invasion and anchorage independent growth, reduces the stemness capacity and increases cell death of HCC cells.
DescriptionResumen del póster presentado al 1st Joint Meeting of the French-Portuguese-Spanish Biochemical and Molecular Biology Societies y al XL Spanish Society of Biochemistry and Molecular Biology (SEBBM) Congress, celebrado en Barcelona (España) del 23 al 26 de octubre de 2017.-- et al.
Appears in Collections:(IBMCC) Comunicaciones congresos
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