Table 1.

Some ESRP1/ESRP2 regulated splice events detected in prostate cancer cells.

GeneGene	Protein Function	ESRP regulation	Clinical relevance
ADAM15	Transmembrane glycoprotein involved in cell adhesion	Activates inclusion of exon 20	ESRP controls poorer prognosis isoform
MINK1	Serine/threonine kinase	Activates inclusion of exon 18	ESRP controls poorer prognosis isoform
MYO1B	Motor protein	Represses exon 23	ESRP controls poorer prognosis isoform
NUMB	Tumour suppressor	Activates inclusion of exon 6	NUMB exon 6 shows more skipping in primary prostate tumours
MLPH	Rab effector protein	Represses exon 9	ESRP controls poorer prognosis isoform
MYH10	Non-muscle actin dependent myosin	Represses exon 6	ESRP controls poorer prognosis isoform
RPS24	needed for cell proliferation	Represses exon 5	ESRP controls poorer prognosis isoform
TUFT1	adaptation to hypoxia, mesenchymal stem cell function, and neuronal differentiation	Activates inclusion of exon 2	ESRP controls poorer prognosis isoform
DOCK7	guanine nucleotide exchange factor	Represses inclusion of exon 23	DOCK7 exon 23 shows more skipping in primary prostate tumours
ARFGAP2	ADP Ribosylation Factor GTPase Activating Protein 2	Activates inclusion of exon 8	ARFGAP2 exon 8 shows more inclusion in primary prostate tumours
ENAH	cell motility and adhesion	Activates inclusion of exon 11A	ENAH exon 11 A shows more inclusion in primary prostate tumours
FN1	cell adhesion and maintenance of cell shape	Represses exon 25
FLNB	Connects cell membrane to actin cytoskeleton	Activates inclusion of exon 30	Exon 30 included form in primary prostate tumours correlates with better prognosis
MAP3K7	controls transcription and apoptosis	Activates inclusion of exon 12	MAP3K7 genetic deletion leads to poor clinical prognosis

This selection of regulated splice events are taken from Munkley et al. 2019 [30] to illustrate how ESRP1/ESRP2 expression levels could control aspects of prostate cancer biology.