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Role of C3G in hepatocarcinoma tumor growth and progression. Regulation of stemness capacity

AuthorsSequera, Celia; Manzano Figueroa, Sara; Arechederra, María; Baquero, Cristina; Guerrero Arroyo, María del Carmen ; Porras, Almudena
Issue Date2016
PublisherSociedad Española de Bioquímica y Biología Molecular
CitationXXXIX Congreso de la SEBBM (2016)
AbstractC3G is a guanine nucleotide exchange factor for Rap1 and R-Ras. It is essential for embryonic development and it 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 different degrees of epithelial phenotypes (Hep3B and HLE), our group found that C3G knock-down increased invasion and migration through induction of an epithelial-mesenchymal transition (EMT) process. Accordingly, C3G knock-down cells expressed higher levels of mesenchymal markers (Vimentin, N-Cadherin) and EMT transcription factors (Snail, Zeb1). All these changes induced by C3G silencing were similar to those elicited by TGF-β, a well known EMT inducer. Based on this pro-migratory effect of C3G knock-down, we have evaluated the role of C3G in tumorigenesis in HCC cells. Anchorage-dependent assays showed reduced number of foci and greater dispersion of cells within a focus in C3G knock-down HCC cells, as compared to parental cells. This correlates with the low adhesion of C3G silenced Hep3B cells. In contrast, anchorage independent assays in soft agar revealed an increase in the number and size of foci in C3G-silenced Hep3B cells, as compared to parental cells. However, each individual focus was composed of few and scattered cells. To further understand the function of C3G in tumor growth, we studied its role on cell survival and found that C3G knock-down decreased cell death. Moreover, our preliminary studies on the role of C3G on stemness capacity of HCC cells showed that C3G knock-down 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. All these data support a role for C3G as an inhibitor of migration and invasion, while its function in tumor growth remains unclear. We are currently evaluating in vivo the role of C3G in HCC tumor growth.
DescriptionResumen del póster presentado al XXXIX Congreso de la Sociedad Española de Bioquímica y Biología Molecular, celebrado en Salamanca del 5 al 8 de septiembre de 2016.
Appears in Collections:(IBMCC) Comunicaciones congresos
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