Cyclin A2, a novel regulator of EMT.Our previous work showed that Cyclin A2 deficiency promotes cell invasion in fibroblasts.  Given that the majority of cancers emerge from epithelia, we explored novel functions for Cyclin A2 by depleting it in normal mammary epithelial cells.  Phenotypes induced by Cyclin A2 deficiency were exacerbated upon oncogenic activated-Ras expression, which led to an increased expression of EMT-related transcriptional factors.  Moreover, Cyclin A2-depleted cells exhibited stem cell-like properties and increased invasion in an in vivo avian embryo model.  Our work supports a model where Cyclin A2 downregulation facilitates cancer cell EMT and metastatic dissemination.
Cyclin A2
Cyclin A2, a novel regulator of EMT.Our previous work showed that Cyclin A2 deficiency promotes cell invasion in fibroblasts.  Given that the majority of cancers emerge from epithelia, we explored novel functions for Cyclin A2 by depleting it in normal mammary epithelial cells.  Phenotypes induced by Cyclin A2 deficiency were exacerbated upon oncogenic activated-Ras expression, which led to an increased expression of EMT-related transcriptional factors.  Moreover, Cyclin A2-depleted cells exhibited stem cell-like properties and increased invasion in an in vivo avian embryo model.  Our work supports a model where Cyclin A2 downregulation facilitates cancer cell EMT and metastatic dissemination.
Cyclin A2
Cyclin A2, a novel regulator of EMT.Our previous work showed that Cyclin A2 deficiency promotes cell invasion in fibroblasts.  Given that the majority of cancers emerge from epithelia, we explored novel functions for Cyclin A2 by depleting it in normal mammary epithelial cells.  Phenotypes induced by Cyclin A2 deficiency were exacerbated upon oncogenic activated-Ras expression, which led to an increased expression of EMT-related transcriptional factors.  Moreover, Cyclin A2-depleted cells exhibited stem cell-like properties and increased invasion in an in vivo avian embryo model.  Our work supports a model where Cyclin A2 downregulation facilitates cancer cell EMT and metastatic dissemination.
Cyclin A2
Cyclin A2, a novel regulator of EMT.Our previous work showed that Cyclin A2 deficiency promotes cell invasion in fibroblasts.  Given that the majority of cancers emerge from epithelia, we explored novel functions for Cyclin A2 by depleting it in normal mammary epithelial cells.  Phenotypes induced by Cyclin A2 deficiency were exacerbated upon oncogenic activated-Ras expression, which led to an increased expression of EMT-related transcriptional factors.  Moreover, Cyclin A2-depleted cells exhibited stem cell-like properties and increased invasion in an in vivo avian embryo model.  Our work supports a model where Cyclin A2 downregulation facilitates cancer cell EMT and metastatic dissemination.
Cyclin A2
Cyclin A2, a novel regulator of EMT.Our previous work showed that Cyclin A2 deficiency promotes cell invasion in fibroblasts.  Given that the majority of cancers emerge from epithelia, we explored novel functions for Cyclin A2 by depleting it in normal mammary epithelial cells.  Phenotypes induced by Cyclin A2 deficiency were exacerbated upon oncogenic activated-Ras expression, which led to an increased expression of EMT-related transcriptional factors.  Moreover, Cyclin A2-depleted cells exhibited stem cell-like properties and increased invasion in an in vivo avian embryo model.  Our work supports a model where Cyclin A2 downregulation facilitates cancer cell EMT and metastatic dissemination.
Cyclin A2