Epithelial specific splicing regulator proteins as emerging oncogenes in aggressive prostate cancer
Research output: Contribution to journal › Review › Research › peer-review
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Epithelial specific splicing regulator proteins as emerging oncogenes in aggressive prostate cancer. / Advani, Rahul; Luzzi, Sara; Scott, Emma; Dalgliesh, Caroline; Weischenfeldt, Joachim; Munkley, Jennifer; Elliott, David J.
In: Oncogene, Vol. 42, 2023, p. 3161-3168.Research output: Contribution to journal › Review › Research › peer-review
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TY - JOUR
T1 - Epithelial specific splicing regulator proteins as emerging oncogenes in aggressive prostate cancer
AU - Advani, Rahul
AU - Luzzi, Sara
AU - Scott, Emma
AU - Dalgliesh, Caroline
AU - Weischenfeldt, Joachim
AU - Munkley, Jennifer
AU - Elliott, David J.
N1 - Publisher Copyright: © 2023, The Author(s).
PY - 2023
Y1 - 2023
N2 - Prostate cancer progression is connected to the activity of conventional oncogenes and tumour suppressors and driven by circulating steroid hormones. A key issue has been how to identify and care for aggressively developing prostate tumours. Here we discuss how expression of the splicing regulators ESRP1 and ESRP2, and how their role as “masterminds” of epithelial splicing patterns, have been identified as markers of aggressively proliferating prostate primary tumours. We suggest that the origin of prostate cancer within epithelial cells, and the subsequent association of ESRP1 and ESRP2 expression with more aggressive disease progression, identify ESRP1 and ESRP2 as lineage survival oncogenes. To move this field on in the future it will be important to identify the gene expression targets controlled by ESRP1/2 that regulate prostate cancer proliferation. Potential future therapies could be designed to target ESRP1 and ESRP2 protein activity or their regulated splice isoforms in aggressive prostate tumours. Design of these therapies is potentially complicated by the risk of producing a more mesenchymal splicing environment that might promote tumour metastasis.
AB - Prostate cancer progression is connected to the activity of conventional oncogenes and tumour suppressors and driven by circulating steroid hormones. A key issue has been how to identify and care for aggressively developing prostate tumours. Here we discuss how expression of the splicing regulators ESRP1 and ESRP2, and how their role as “masterminds” of epithelial splicing patterns, have been identified as markers of aggressively proliferating prostate primary tumours. We suggest that the origin of prostate cancer within epithelial cells, and the subsequent association of ESRP1 and ESRP2 expression with more aggressive disease progression, identify ESRP1 and ESRP2 as lineage survival oncogenes. To move this field on in the future it will be important to identify the gene expression targets controlled by ESRP1/2 that regulate prostate cancer proliferation. Potential future therapies could be designed to target ESRP1 and ESRP2 protein activity or their regulated splice isoforms in aggressive prostate tumours. Design of these therapies is potentially complicated by the risk of producing a more mesenchymal splicing environment that might promote tumour metastasis.
U2 - 10.1038/s41388-023-02838-9
DO - 10.1038/s41388-023-02838-9
M3 - Review
C2 - 37752235
AN - SCOPUS:85172168426
VL - 42
SP - 3161
EP - 3168
JO - Oncogene
JF - Oncogene
SN - 0950-9232
ER -
ID: 368904699