An amendment to this paper has been published and can be accessed via a link at the top of the paper

A Dutton

A Lollies

A Muto

A Rosenwald

BM Bolstad

BT Edelson

C Steidl

F. Jundt

FA Scheeren

FL Scott

G Cattoretti

GK Smyth

GM Reynolds

H Han

H Le Stunff

H Okamoto

I Inoki

I Schwering

J De

J Heather

J Ye

JA Green

JA Reusch

JF Garcia

JM Vaquerizas

JR Flavell

K Arikawa

K Hildner

K Nie

K Ochiai

K Vrzalikova

LB Justement

LL Laichalk

M Buettner

M Iacobelli

M Jucker

M Vockerodt

MG Bayerl

MJ Kluk

NC Hait

PJ Farrell

PJ Lane

PM Lieberman

RA Irizarry

S Leonard

S Milstien

S Pan

SM Mandala

T Sanchez

V Brune

W Du

WH Moolenaar

XY Gao

Y Takuwa

English

Crossref

Correction: S1PR1 drives a feedforward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells

The Hodgkin/Reed–Sternberg cells of classical Hodgkin lymphoma (HL) are characterised by the aberrant activation of multiple signalling pathways. Here we show that a subset of HL displays altered expression of sphingosine-1-phosphate (S1P) receptors (S1PR)s. S1P activates phosphatidylinositide 3-kinase (PI3-K) in these cells that is mediated by the increased expression of S1PR1 and the decreased expression of S1PR2. We also showed that genes regulated by the PI3-K signalling pathway in HL cell lines significantly overlap with the transcriptional programme of primary HRS cells. Genes upregulated by the PI3-K pathway included the basic leucine zipper transcription factor, ATF-like 3 (BATF3), which is normally associated with the development of dendritic cells. Immunohistochemistry confirmed that BATF3 was expressed in HRS cells of most HL cases. In contrast, in normal lymphoid tissues, BATF3 expression was confined to a small fraction of CD30-positive immunoblasts. Knockdown of BATF3 in HL cell lines revealed that BATF3 contributed to the transcriptional programme of primary HRS cells, including the upregulation of S1PR1. Our data suggest that disruption of this potentially oncogenic feedforward S1P signalling loop could provide novel therapeutic opportunities for patients with HL

Vrzalikova, K

Ibrahim, M

Vockerodt, M

Perry, T

Margielewska, S

Lupino, L

Nagy, E

Soilleux, E

Liebelt, D

Hollows, R

Last, A

Reynolds, G

Abdullah, M

Curley, H

Care, M

Krappmann, D

Tooze, R

Allegood, J

Spiegel, S

Wei, W

Woodman, CBJ

Murray, PG

White Rose Research Online

S1PR1 drives a feedforward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells

The Hodgkin/Reed-Sternberg cells of classical Hodgkin lymphoma (HL) are characterised by the aberrant activation of multiple signalling pathways. Here we show that a subset of HL displays altered expression of sphingosine-1-phosphate (S1P) receptors (S1PR)s. S1P activates phosphatidylinositide 3-kinase (PI3-K) in these cells that is mediated by the increased expression of S1PR1 and the decreased expression of S1PR2. We also showed that genes regulated by the PI3-K signalling pathway in HL cell lines significantly overlap with the transcriptional programme of primary HRS cells. Genes upregulated by the PI3-K pathway included the basic leucine zipper transcription factor, ATF-like 3 (BATF3), which is normally associated with the development of dendritic cells. Immunohistochemistry confirmed that BATF3 was expressed in HRS cells of most HL cases. In contrast, in normal lymphoid tissues, BATF3 expression was confined to a small fraction of CD30-positive immunoblasts. Knockdown of BATF3 in HL cell lines revealed that BATF3 contributed to the transcriptional programme of primary HRS cells, including the upregulation of S1PR1. Our data suggest that disruption of this potentially oncogenic feedforward S1P signalling loop could provide novel therapeutic opportunities for patients with HL

Vrzalikova, K.

Ibrahim, M.M.

Vockerodt, M.

Perry, T.E.

Margielewska, S.

Lupino, L.

Nagy, E.

Soilleux, E.

Liebelt, D.

Hollows, R.

Last, A.

Reynolds, G.

Abdullah, M.

Curley, H.

Care, M.

Krappmann, D.

Tooze, R.

Allegood, J.

Spiegel, S.

Wei, W.

Woodman, C.B.J.

Murray, P.G.

PuSH

S1PR1 drives a feedforward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells.

Vrzalikova, Katerina

Ibrahim, M.

Vockerodt, Martina

Perry, Tracy

Nagy, Ester

Abdullah, Maizatul Atmadini

Woodman, C. B. J.

Murray, Paul G.

Universiti Putra Malaysia Institutional Repository

S1PR1 drives a feed forward signaling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells ABSTRACT The Hodgkin/Reed-Sternberg cells of classical Hodgkin lymphoma (HL) are characterised by the aberrant activation of multiple signalling pathways. Here we show that a subset of HL displays altered expression of sphingosine-1-phosphate (S1P) receptors (S1PR)s. S1P activates phosphatidylinositide 3-kinase (PI3-K) in these cells that is mediated by the increased expression of S1PR1 and the decreased expression of S1PR2. We also showed that genes regulated by the PI3-K signalling pathway in HL cell lines significantly overlap with the transcriptional programme of primary HRS cells. Genes upregulated by the PI3-K pathway included the basic leucine zipper transcription factor, ATF-like 3 (BATF3), which is normally associated with the development of dendritic cells. Immunohistochemistry confirmed that BATF3 was expressed in HRS cells of most HL cases. In contrast, in normal lymphoid tissues, BATF3 expression was confined to a small fraction of CD30-positive immunoblasts. Knockdown of BATF3 in HL cell lines revealed that BATF3 contributed to the transcriptional programme of primary HRS cells, including the upregulation of S1PR1. Our data suggest that disruption of this potentially oncogenic feedforward S1P signalling loop could provide novel therapeutic opportunities for patients with HL. 

S1PR1 drives a feed forward signaling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells

The Hodgkin/Reed-Sternberg (HRS) cells of classical Hodgkin lymphoma (HL) are characterised by the aberrant activation of multiple signalling pathways. Here we show that a subset of HL displays altered expression of sphingosine-1-phosphate (S1P) receptors (S1PR). S1P activates phosphatidylinositide 3-kinase (PI3-K) in these cells that is mediated by the increased expression of S1PR1 and the decreased expression of S1PR2. We also showed that genes regulated by PI3-K signalling pathway in HL cell lines significantly overlap with the transcriptional programme of primary HRS cells. Genes up-regulated by the PI3-K pathway included the basic leucine zipper transcription factor, ATF-like 3 (BATF3), which is normally associated with the development of dendritic cells. Immunohistochemistry confirmed that BATF3 was expressed in HRS cells of most HL cases. In contrast, in normal lymphoid tissues, BATF3 expression was confined to a small fraction of CD30-positive immunoblasts. Knockdown of BATF3 in HL cell lines revealed that BATF3 contributed to the transcriptional programme of primary HRS cells, including the upregulation of S1PR1. Our data suggest that disruption of this potentially oncogenic feed-forward S1P signalling loop could provide novel therapeutic opportunities for patients with HL.Leukemia accepted article preview online, 07 September 2017. doi:10.1038/leu.2017.275

Perry, T.

S1PR1 drives a feed forward signalling loop to regulate BATF3 and the transcriptional programme of hodgkin lymphoma cells

Murray, P. G.

S1PR1 drives a feedforward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells  ABSTRACT  The Hodgkin/Reed–Sternberg cells of classical Hodgkin lymphoma (HL) are characterised by the aberrant activation of multiple signalling pathways. Here we show that a subset of HL displays altered expression of sphingosine-1-phosphate (S1P) receptors (S1PR)s. S1P activates phosphatidylinositide 3-kinase (PI3-K) in these cells that is mediated by the increased expression of S1PR1 and the decreased expression of S1PR2. We also showed that genes regulated by the PI3-K signalling pathway in HL cell lines significantly overlap with the transcriptional programme of primary HRS cells. Genes upregulated by the PI3-K pathway included the basic leucine zipper transcription factor, ATF-like 3 (BATF3), which is normally associated with the development of dendritic cells. Immunohistochemistry confirmed that BATF3 was expressed in HRS cells of most HL cases. In contrast, in normal lymphoid tissues, BATF3 expression was confined to a small fraction of CD30-positive immunoblasts. Knockdown of BATF3 in HL cell lines revealed that BATF3 contributed to the transcriptional programme of primary HRS cells, including the upregulation of S1PR1. Our data suggest that disruption of this potentially oncogenic feedforward S1P signalling loop could provide novel therapeutic opportunities for patients with HL. Keyword:  Hodgkin lymphoma; Lymphoid; Sphingosine-1-phosphate (S1P); Sphingosine kinase 1 (SPHK1)       

S1PR1 drives a feedforward signaling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells

Ibrahim, Maha

Perry, Tracey

Margielewska, Sandra

Lupino, Lauren

Nagy, Eszter

Soilleux, Elizabeth

Liebelt, Daniela

Hollows, Robert

Last, Amanda

Reynolds, Gary

Abdullah, Maizaton

Curley, Helen

Care, Mathew

Krappmann, Daniel

Tooze, Reuben

Allegood, Jeremy

Spiegel, Sarah

Wei, Wenbin

Woodman, Ciaran

Murray, Paul

University of Birmingham Research Portal

M Ibrahim

T Perry

S Margielewska

L Lupino

E Nagy

E Soilleux

D Liebelt

R Hollows

A Last

G Reynolds

M Abdullah

H Curley

M Care

D Krappmann

R Tooze

J Allegood

S Spiegel

W Wei

C B J Woodman

P G Murray

Leukemia

Apollo (Cambridge)

Leukemia (2019) 33:2126https://doi.org/10.1038/s41375-019-0511-zCORRECTIONCorrection: S1PR1 drives a feedforward signalling loop to regulateBATF3 and the transcriptional programme of Hodgkin lymphomacellsK Vrzalikova1 ● M Ibrahim1 ● M Vockerodt1,2 ● T Perry1 ● S Margielewska1 ● L Lupino1 ● E Nagy1 ● E Soilleux3 ●D Liebelt1 ● R Hollows1 ● A Last1 ● G Reynolds4 ● M Abdullah1,5 ● H Curley1 ● M Care6 ● D Krappmann7 ● R Tooze6 ●J Allegood8 ● S Spiegel8 ● W Wei1,9 ● C B J Woodman1 ● P G Murray1,10Published online: 25 June 2019© The Author(s) 2019. This article is published with open accessCorrection to: Leukemiahttps://doi.org/10.1038/leu.2017.275This article was originally published under a CC BY-NC-ND 4.0 license, but has now been made available under aCC-BY 4.0 license.Open Access This article is licensed under a Creative CommonsAttribution 4.0 International License, which permits use, sharing,adaptation, distribution and reproduction in any medium or format, aslong as you give appropriate credit to the original author(s) and thesource, provide a link to the Creative Commons license, and indicate ifchanges were made. The images or other third party material in thisarticle are included in the article’s Creative Commons license, unlessindicated otherwise in a credit line to the material. If material is notincluded in the article’s Creative Commons license and your intendeduse is not permitted by statutory regulation or exceeds the permitteduse, you will need to obtain permission directly from the copyrightholder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.* P G Murrayp.g.murray@bham.ac.uk1 Institute of Cancer and Genomic Sciences, University ofBirmingham, Birmingham, UK2 Institute of Anatomy and Cell Biology, Georg-August Universityof Göttingen, Göttingen, Germany3 Department of Cellular Pathology, John Radcliffe Hospital,Oxford, UK4 Institute of Immunology and Immunotherapy, University ofBirmingham, Birmingham, UK5 Department of Pathology, Universiti Putra Malaysia,Selangor, Malaysia6 Leeds Institute of Cancer and Pathology, University of Leeds,Leeds, UK7 Research Unit Cellular Signal Integration, Helmholtz ZentrumMünchen, Neuherberg, Germany8 Department of Biochemistry and Molecular Biology and MasseyCancer Center, Virginia Commonwealth University School ofMedicine, Richmond, VA, USA9 Sheffield Institute of Translational Neuroscience, University ofSheffield, Sheffield, UK10 Department of Clinical and Molecular Pathology, Institute ofMolecular and Translational Medicine, Faculty of Medicine andDentistry, Palacky University, Olomouc, Czech Republic1234567890();,:1234567890();,:

Correction: S1PR1 drives a feedforward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells.

S1PR1 drives a feedforward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells (vol 32, pg 214, 2018).

https://eprints.whiterose.ac.uk/121322/1/leu2017275a.pdf

Correction: S1PR1 drives a feedforward signalling loop to regulate BATF3 and the transcriptional programme of Hodgkin lymphoma cells.

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