Regulation of Phosphoglucose Isomerase/Autocrine Motility Factor Activities by the Poly(ADP-Ribose) Polymerase Family-14

Yanagawa, Takashi; Funasaka, Tatsuyoshi; Tsutsumi, Soichi; Hu, Huankai; Watanabe, Hideomi; Raz, Avraham

doi:10.1158/0008-5472.can-07-1586

Cited by 31 publications

(28 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Akt acts in part by phosphorylating GSK3β and the transcription factors Foxo1 and 3a (21). Although PARP14 has been reported to influence protein stability (16), absolute levels and IL-4-induced phosphorylation of these downstream targets of Akt were intact in PARP14-and Stat6-null B cells (Fig. 1D).…”

Section: Parp14mentioning

confidence: 90%

See 1 more Smart Citation

Glycolytic rate and lymphomagenesis depend on PARP14, an ADP ribosyltransferase of the B aggressive lymphoma (BAL) family

Cho¹,

Ahn²,

Bhargava

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

128

View full text Add to dashboard Cite

Poly(ADP-ribose)polymerase (PARP)14-a member of the B aggressive lymphoma (BAL) family of macrodomain-containing PARPs-is an ADP ribosyltransferase that interacts with Stat6, enhances induction of certain genes by IL-4, and is expressed in B lymphocytes. We now show that IL-4 enhancement of glycolysis in B cells requires PARP14 and that this process is central to a role of PARP14 in IL-4-induced survival. Thus, enhancements of AMP-activated protein kinase activity restored both IL-4-induced glycolytic activity in Parp14 −/− B cells and prosurvival signaling by this cytokine. Suppression of apoptosis is central to B-lymphoid oncogenesis, and elevated macro-PARP expression has been correlated with lymphoma aggressiveness. Strikingly, PARP14 deficiency delayed B lymphomagenesis and reversed the block to B-cell maturation driven by the Myc oncogene. Collectively, these findings reveal links between a mammalian ADP ribosyltransferase, cytokine-regulated metabolic activity, and apoptosis; show that PARP14 influences Myc-induced oncogenesis; and suggest that the PARP14-dependent capacity to increase cellular metabolic rates may be an important determinant of lymphoma pathobiology.

show abstract

Section: Parp14mentioning

confidence: 90%

“…These findings suggest that PARP14 is a coactivator of Stat6 at some target genes. Other work in a sarcoma cell line determined that human PARP14 regulates the ubiquitination and levels of phosphoglucose isomerase, a protein involved in intermediary metabolism (16). These latter results suggested a potential link between PARP14 and cellular metabolism.…”

mentioning

confidence: 88%

Glycolytic rate and lymphomagenesis depend on PARP14, an ADP ribosyltransferase of the B aggressive lymphoma (BAL) family

Cho¹,

Ahn²,

Bhargava

et al. 2011

Proc. Natl. Acad. Sci. U.S.A.

128

View full text Add to dashboard Cite

show abstract

“…: T5618). The rabbit anti-ARTD8 antibody was a generous gift from Dr. Avraham Raz (Karmanos Cancer Institute, School of Medicine, Wayne State University, Detroit, Michigan 48201, USA [99]). Immunofluorescence analysis was performed with an automated inverted research microscope system (Leica DMI6000B, Leica Microsystem).…”

Section: Methodsmentioning

confidence: 99%

DTX3L and ARTD9 inhibit IRF1 expression and mediate in cooperation with ARTD8 survival and proliferation of metastatic prostate cancer cells

et al. 2014

View full text Add to dashboard Cite

BackgroundProstate cancer (PCa) is one of the leading causes of cancer-related mortality and morbidity in the aging male population and represents the most frequently diagnosed malignancy in men around the world. The Deltex (DTX)-3-like E3 ubiquitin ligase (DTX3L), also known as B-lymphoma and BAL-associated protein (BBAP), was originally identified as a binding partner of the diphtheria-toxin-like macrodomain containing ADP-ribosyltransferase-9 (ARTD9), also known as BAL1 and PARP9. We have previously demonstrated that ARTD9 acts as a novel oncogenic survival factor in high-risk, chemo-resistant, diffuse large B cell lymphoma (DLBCL). The mono-ADP-ribosyltransferase ARTD8, also known as PARP14 functions as a STAT6-specific co-regulator of IL4-mediated proliferation and survival in B cells.MethodsCo-expression of DTX3L, ARTD8, ARTD9 and STAT1 was analyzed in the metastatic PCa (mPCa) cell lines PC3, DU145, LNCaP and in the normal prostate luminal epithelial cell lines HPE and RWPE1. Effects on cell proliferation, survival and cell migration were determined in PC3, DU145 and/or LNCaP cells depleted of DTX3L, ARTD8, ARTD9, STAT1 and/or IRF1 compared to their proficient control cells, respectively. In further experiments, real-time RT-PCR, Western blot, immunofluorescence and co-immunoprecipitations were conducted to evaluate the physical and functional interactions between DTX3L, ARTD8 and ARTD9.ResultsHere we could identify DTX3L, ARTD9 and ARTD8 as novel oncogenic survival factors in mPCa cells. Our studies revealed that DTX3L forms a complex with ARTD8 and mediates together with ARTD8 and ARTD9 proliferation, chemo-resistance and survival of mPCa cells. In addition, DTX3L, ARTD8 and ARTD9 form complexes with each other. Our study provides first evidence that the enzymatic activity of ARTD8 is required for survival of mPCa cells. DTX3L and ARTD9 act together as repressors of the tumor suppressor IRF1 in mPCa cells. Furthermore, the present study shows that DTX3L together with STAT1 and STAT3 is implicated in cell migration of mPCa cells.ConclusionsOur data strongly indicate that a crosstalk between STAT1, DTX3L and ARTD-like mono-ADP-ribosyltransferases mediates proliferation and survival of mPCa cells. The present study further suggests that the combined targeted inhibition of STAT1, ARTD8, ARTD9 and/or DTX3L could increase the efficacy of chemotherapy or radiation treatment in prostate and other high-risk tumor types with an increased STAT1 signaling.

show abstract

“…Immunoblot procedures and immunofluorescence microscopy were performed as described previously (Guetg et al, 2012;Hassa et al, 2005) using the following primary antibodies: monoclonal mouse anti-HA and mouse anti-FLAG antibodies (both Sigma), polyclonal rabbit anti-BAL1 antibodies (C-terminal; Millipore), monoclonal rabbit anti-STAT1, anti-pSTAT1(Y701), anti-pSTAT1(S727), anti-STAT2, anti-pSTAT2(Y690), anti-IRF2, anti-BLIMP1, anti-Casp3, anti-BCL2, anti-BAD, anti-BAD-S112, anti-PIM1, anti-PIM2, anti-PTBN1, anti-JAK1, antipJAK1, anti-JAK2, anti-pJAK2, anti-IFNGR1, anti-PTBN2 and anti-BCL-XL antibodies (RabMab, Epitomics), monoclonal rabbit anti-IRF1 (RabMab, Cell Signaling Technology), monoclonal mouse anti-tubulin, polyclonal rabbit anti-p53 and anti-BCL6 antibodies (Santa Cruz Biotechnology). The polyclonal rabbit anti-BAL2/ARTD8 antibody was a generous gift from Avraham Raz (Karmanos Cancer Institute, School of Medicine, Wayne State University, Detroit, Michigan 48201, USA) (Yanagawa et al, 2007). Immunofluorescently stained cells were analyzed by fluorescence microscopy on a Leica DMI6000B automated inverted research microscope system (Leica Microsystem).…”

Section: Interaction Assays Immunoblot Analysis and Immunofluorescenmentioning

confidence: 99%

BAL1/ARTD9 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-53 axes in diffuse large B-cell lymphoma

Camicia

Bachmann

Winkler

et al. 2013

Journal of Cell Science

100

View full text Add to dashboard Cite

SummaryThe B-aggressive lymphoma-1 protein and ADP-ribosyltransferase BAL1/ARTD9 has been recently identified as a risk-related gene product in aggressive diffuse large B-cell lymphoma (DLBCL). BAL1 is constitutively expressed in a subset of high-risk DLBCLs with an active host inflammatory response and has been suggested to be associated with interferon-related gene expression. Here we identify BAL1 as a novel oncogenic survival factor in DLBCL and show that constitutive overexpression of BAL1 in DLBCL tightly associates with intrinsic interferon-gamma (IFNc) signaling and constitutive activity of signal transducer and activator of transcription (STAT)-1. Remarkably, BAL1 stimulates the phosphorylation of both STAT1 isoforms, STAT1a and STAT1b, on Y701 and thereby promotes the nuclear accumulation of the antagonistically acting and transcriptionally repressive isoform STAT1b. Moreover, BAL1 physically interacts with both STAT1a and STAT1b through its macrodomains in an ADP-ribosylation-dependent manner. BAL1 directly inhibits, together with STAT1b, the expression of tumor suppressor and interferon response factor (IRF)-1. Conversely, BAL1 enhances the expression of the proto-oncogenes IRF2 and B-cell CLL/lymphoma (BCL)-6 in DLBCL. Our results show for the first time that BAL1 represses the anti-proliferative and pro-apoptotic IFNc-STAT1-IRF1-p53 axis and mediates proliferation, survival and chemoresistance in DLBCL. As a consequence constitutive IFNc-STAT1 signaling does not lead to apoptosis but rather to chemo-resistance in DLBCL overexpressing BAL1. Our results suggest that BAL1 may induce an switch in STAT1 from a tumor suppressor to an oncogene in high-risk DLBCL.

show abstract

Regulation of Phosphoglucose Isomerase/Autocrine Motility Factor Activities by the Poly(ADP-Ribose) Polymerase Family-14

Abstract: Phosphoglucose isomerase (PGI; EC 5.3

Cited by 31 publications

References 45 publications

Glycolytic rate and lymphomagenesis depend on PARP14, an ADP ribosyltransferase of the B aggressive lymphoma (BAL) family

Glycolytic rate and lymphomagenesis depend on PARP14, an ADP ribosyltransferase of the B aggressive lymphoma (BAL) family

DTX3L and ARTD9 inhibit IRF1 expression and mediate in cooperation with ARTD8 survival and proliferation of metastatic prostate cancer cells

BAL1/ARTD9 represses the anti-proliferative and pro-apoptotic IFNγ-STAT1-IRF1-53 axes in diffuse large B-cell lymphoma

Contact Info

Product

Resources

About