ETS transcription factor ELF3 (ESE‐1) is a cell cycle regulator in benign and malignant prostate. Issue 7 (6th May 2022)

• Record Type: Journal Article
• Authors: Archer, Leanne K.; Frame, Fiona M.; Walker, Hannah F.; Droop, Alastair P.; McDonald, Georgina L. K.; Kucko, Samuel; Berney, Daniel M.; Mann, Vincent M.; Simms, Matthew S.; Maitland, Norman J.
• Is Part Of: FEBS open bio. Volume 12:Issue 7(2022)
• Page Start: 1365
• Page End: 1387
• Publication Date: 2022-05-06
• Subjects: cell cycle -- ELF3 -- patient samples -- prostate -- prostate cancer -- siRNA; Molecular biology -- Periodicals; Cytology -- Periodicals; Life sciences -- Periodicals; Biological Science Disciplines -- Periodicals; Molecular Biology -- Periodicals; Cell Biology -- Periodicals; Cytology; Life sciences; Molecular biology; Periodicals; 572.805
• DOI: 10.1002/2211-5463.13417
• Languages: English
• ISSNs: 2211-5463

Abstract

Abstract : This study aimed to elucidate the role of ELF3, an ETS family member in normal prostate growth and prostate cancer. Silencing ELF3 in both benign prostate (BPH‐1) and prostate cancer (PC3) cell lines resulted in decreased colony‐forming ability, inhibition of cell migration and reduced cell viability due to cell cycle arrest, establishing ELF3 as a cell cycle regulator. Increased ELF3 expression in more advanced prostate tumours was shown by immunostaining of tissue microarrays and from analysis of gene expression and genetic alteration studies. This study indicates that ELF3 functions not only as a part of normal prostate epithelial growth but also as a potential oncogene in advanced prostate cancers. Abstract : In the prostate, ELF3 is expressed in committed basal (CB) cells but not stem cells (SC), transit amplifying (TA) cells or luminal (L) cells. Using siRNA to knockdown ELF3 expression results in cell cycle arrest, reduced colony formation and reduced wound healing. ELF3 is expressed in some high grade cancers and there is evidence for ELF3 amplification in metastatic cancers.