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Regulation of the alternative splicing of RAC1B in tumor cells
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Resumo(s)
A subgroup of colon tumors is characterized by the simultaneous presence of an oncogenic mutation in BRAF and overexpression of RAC1B, a splicing variant of the GTPase RAC1. RAC1B overexpression has also been identified in pancreatic, breast, lung and thyroid cancer. Inclusion of alternative exon 3b originates variant protein RAC1B and depends on two splicing factors, SRSF1 and SRSF3, which promote and inhibit, respectively, inclusion of this exon in colorectal cancer cells. ESRP1 has also been found to promote RAC1B expression in these cells. Here we studied whether these 3 splicing factors are also modulators of alternative splicing of RAC1B in breast and lung cancer cells.
A similar role for SRSF1 and SRSF3 was found in breast cancer cells. Intriguingly, ESRP1 revealed an opposite role in alternative splicing of RAC1B comparing to what was previously observed in colorectal cancer cells. Currently, we are extending this study to lung cancer cells.
Descrição
Palavras-chave
Vias de Transdução de Sinal e Patologias Associadas RAC1B Cancer Alternative Splicing