KLF9 and ESR1 crosstalk in ESR1 signalling

Increased risk for endometrial cancers is associated with inappropriate early exposure to oestrogenic compounds. Although dysregulation of ESR1 signalling is acknowledged to mediate early events in tumor initiation, mechanisms contributing to sustained ESR1 activity later in life and leading to induction of oncogenic pathways remain poorly understood.

Simmons et al. evaluated the contribution of the transcription factor, KLF9 to early perturbations in uterine ESR1 signalling pathways induced by diethylstilbestrol. Their in vivo model revealed a molecular network between KLF9 and ESR1 involving key oestrogen-regulated genes. The results raise the intriguing possibility that silencing KLF9 could contribute to increased susceptibility for developing endometrial cancers initiated by aberrant oestrogen activity. Simmons et al. (2010), Journal of Endocrinology.

Read the full article at DOI:10.1677/JOE-09-0474