TY - JOUR
T1 - PHF19 mediated regulation of proliferation and invasiveness in prostate cancer cells
AU - Jain, Payal
AU - Ballare, Cecilia
AU - Blanco, Enrique
AU - Vizan, Pedro
AU - Di Croce, Luciano
N1 - Funding Information:
The work in the Di Croce laboratory is supported by grants from the Spanish Ministry of Science and Innovation (AEI, BFU2016-75008-P), “Fundación Vencer El Cancer” (VEC), the European Regional Development Fund (ERDF), Fundació “La Marató de TV3”, and from Secretaria d’Universi-tats i Recerca del Departament d’Economia I Coneixement de la Generalitat de Catalunya (AGAUR, 2017 SGR). PV was supported by “Fundación Científica de la Asociación Española Contra el Cán-cer”. We acknowledge support of the Spanish Ministry of Science and Innovation through the Insti-tuto de Salud Carlos III and to the EMBL partnership; Centro de Excelencia Severo Ochoa; CERCA Programme / Generalitat de Catalunya.
Publisher Copyright:
© Jain et al.
PY - 2020/3
Y1 - 2020/3
N2 - The Polycomb-like protein PHF19/PCL3 associates with PRC2 and mediates its recruitment to chromatin in embryonic stem cells. PHF19 is also overexpressed in many cancers. However, neither PHF19 targets nor misregulated pathways involving PHF19 are known. Here, we investigate the role of PHF19 in prostate cancer cells. We find that PHF19 interacts with PRC2 and binds to PRC2 targets on chromatin. PHF19 target genes are involved in proliferation, differentiation, angiogenesis, and extracellular matrix organization. Depletion of PHF19 triggers an increase in MTF2/PCL2 chromatin recruitment, with a genome-wide gain in PRC2 occupancy and H3K27me3 deposition. Transcriptome analysis shows that PHF19 loss promotes deregulation of key genes involved in growth, metastasis, invasion, and of factors that stimulate blood vessels formation. Consistent with this, PHF19 silencing reduces cell proliferation, while promotes invasive growth and angiogenesis. Our findings reveal a role for PHF19 in controlling the balance between cell proliferation and invasiveness in prostate cancer.
AB - The Polycomb-like protein PHF19/PCL3 associates with PRC2 and mediates its recruitment to chromatin in embryonic stem cells. PHF19 is also overexpressed in many cancers. However, neither PHF19 targets nor misregulated pathways involving PHF19 are known. Here, we investigate the role of PHF19 in prostate cancer cells. We find that PHF19 interacts with PRC2 and binds to PRC2 targets on chromatin. PHF19 target genes are involved in proliferation, differentiation, angiogenesis, and extracellular matrix organization. Depletion of PHF19 triggers an increase in MTF2/PCL2 chromatin recruitment, with a genome-wide gain in PRC2 occupancy and H3K27me3 deposition. Transcriptome analysis shows that PHF19 loss promotes deregulation of key genes involved in growth, metastasis, invasion, and of factors that stimulate blood vessels formation. Consistent with this, PHF19 silencing reduces cell proliferation, while promotes invasive growth and angiogenesis. Our findings reveal a role for PHF19 in controlling the balance between cell proliferation and invasiveness in prostate cancer.
UR - http://www.scopus.com/inward/record.url?scp=85081928191&partnerID=8YFLogxK
U2 - 10.7554/eLife.51373
DO - 10.7554/eLife.51373
M3 - Article
C2 - 32155117
AN - SCOPUS:85081928191
SN - 2050-084X
VL - 9
JO - eLife
JF - eLife
M1 - e51373
ER -