Poly(ADP-ribosyl)ation is implicated in the G0–G1 transition of resting cells

Carbone, Mariarosaria; Rossi, Marianna Nicoletta; Cavaldesi, Michaela; Notari, Airton Carlos; Amati, Paolo; Maione, Rossella

doi:10.1038/onc.2008.221

Cited by 34 publications

(34 citation statements)

References 35 publications

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“…Additionally, the ability to bind PARP-1 when automodified with PAR chains distinguishes macroH2A1.1 from macroH2A1.2. Finally, PARP activity has been linked to cell cycle progression through several disparate mechanisms (7,(15)(16)(17)22). Strikingly, we found that PARP-1 levels, both full-length and p89, were specifically reduced in macroH2A1.1-expressing cells (Fig.…”

Section: ϫ12mentioning

confidence: 51%

QKI-Mediated Alternative Splicing of the Histone Variant MacroH2A1 Regulates Cancer Cell Proliferation

Novikov

Park

Chen

et al. 2011

Molecular and Cellular Biology

144

163

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The histone variant macroH2A1 contains a carboxyl-terminal ϳ30-kDa domain called a macro domain. MacroH2A1 is produced as one of two alternatively spliced forms, macroH2A1.1 and macroH2A1.2. While the macro domain of macroH2A1.1 can interact with NAD ؉ -derived small molecules, such as poly(ADP-ribose), macroH2A1.2's macro domain cannot. Here, we show that changes in the alternative splicing of macroH2A1 pre-mRNA, which lead to a decrease in macroH2A1.1 expression, occur in a variety of cancers, including testicular, lung, bladder, cervical, breast, colon, ovarian, and endometrial. Furthermore, reintroduction of macroH2A1.1 suppresses the proliferation of lung and cervical cancer cells in a manner that requires the ability of macroH2A1.1 to bind NAD ؉ -derived metabolites. MacroH2A1.1-mediated suppression of proliferation occurs, at least in part, through the reduction of poly(ADP-ribose) polymerase 1 (PARP-1) protein levels. By analyzing publically available expression and splicing microarray data, we identified splicing factors that correlate with alterations in macroH2A1 splicing. Using RNA interference, we demonstrate that one of these factors, QKI, regulates the alternative splicing of macroH2A1 pre-mRNA, resulting in increased levels of macroH2A1.1. Finally, we demonstrate that QKI expression is significantly reduced in many of the same cancer types that demonstrate a reduction in macroH2A1.1 splicing.

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Section: ϫ12mentioning

confidence: 51%

QKI-Mediated Alternative Splicing of the Histone Variant MacroH2A1 Regulates Cancer Cell Proliferation

Novikov

Park

Chen

et al. 2011

Molecular and Cellular Biology

144

163

View full text Add to dashboard Cite

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“…c Myc can indirectly increase Parp1 activity through decreasing BIN1, a nucleocytoplasmic adaptor protein that binds Parp1 and suppresses its catalytic activity (Pyndiah et al, 2011). Carbone et al (2008) also demonstrated that Parp1 and PARylation modulate the induction of c Myc in serum stimulated quies cent fibroblasts. However, whether Parp1 is also a regulator of c Myc in pluripotent stem cells still remained undetermined.…”

Section: Discussionmentioning

confidence: 99%

Poly(ADP-ribose) polymerase 1 regulates nuclear reprogramming and promotes iPSC generation without c-Myc

Chiou¹,

Jiang²,

Yu³

et al. 2013

J Cell Biol

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85Somatic cell reprogramming is a promising strat egy for stem cell biology and regenerative medicine. Accumulated data have shown that nuclear reprogramming can be experimentally induced by three methods: nuclear transfer, cell fusion, or forced expression of transcription factors (Yamanaka and Blau, 2010). It is con ceivable that mature oocytes and embryonic stem cells (ESCs) contain reprogramming fac tors (proteins, RNAs, lipids, and small mole cules) that enable these somatic cells to undergo efficient nuclear reprogramming, a process of converting somatic cells to pluripotent states (Jullien et al., 2010;Wang et al., 2010). Recent evidence has emphasized the pivotal roles of nuclear proteins in the regulation of chromatin remodeling and epigenetic modifications during the reprogramming process . However, the precise molecular mechanisms of the regulation of nuclear factors during cellular reprogramming remain uncertain.Induced pluripotent stem cells (iPSCs) are a recently developed technology that holds promise for stem cell biology and regenerative medicine (Takahashi et al., 2007;Nakagawa et al., 2008). Nuclear reprogramming induced by trans cription factors resets the epigenetic landmarks, which leads to the global reversion of the somatic

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“…Negroni et al 23 showed that mitogen-stimulated human lymphocytes had 20-fold higher levels of PARP1 mRNA compared to quiescent lymphocytes. More recently, Carbone et al 24 demonstrated that PARP-1 activity was induced by mitogen stimulation and contributed to the G0-G1 cell cycle transition via the induction of immediate-early genes such as c-Myc and c-Fos. In addition, there is strong evidence in the literature showing that PARP expression and activity are affected by differentiation and cell proliferation with generally higher PARP activity and expression in proliferating cells.…”

Section: Discussionmentioning

confidence: 99%

Variations in the mRNA expression of poly(ADP‐ribose) polymerases, poly(ADP‐ribose) glycohydrolase and ADP‐ribosylhydrolase 3 in breast tumors and impact on clinical outcome

Bièche

Pennaneach

Driouch

et al. 2013

Intl Journal of Cancer

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In order to assess the variation in expression of poly(ADP-ribose) polymerase (PARP) family members and the hydrolases that degrade the poly(ADP-ribose) polymers they generate and possible associations with classical pathological parameters, including long-term outcome, the mRNA levels of PARP1, PARP2, PARP3, poly(ADP-ribose) glycohydrolase (PARG) and ADP-ribosylhydrolase 3 (ARH3) were examined using quantitative reverse transcription polymerase chain reaction in 443 unilateral invasive breast cancers and linked to hormonal status, tumor proliferation and clinical outcome. PARP1 mRNA levels were the highest among these five genes in both normal and tumor tissues, with a 2.45-fold higher median level in tumors compared to normal tissues. Tumors (34.1%) showed PARP1 overexpression (>3 fold relative to normal breast tissues) compared to underexpression (<0.33 fold) in only 0.5%. This overexpression was seen in all breast tumor subgroups, with the highest fraction (51%) seen in the HR-positive/ERBB2-positive subgroup and was not highly associated with any other classical predictive factors. No correlation was seen between PARP1 mRNA and PARP-1 protein levels in a subset of 31 tumors. PARP3 was underexpressed in 10.4% of tumors, more frequently in the HR-negative tumors (25.4%) than the HR-positive tumors (5.9%). This PARP3 underexpression was mutually exclusive with a PARP1 overexpression. PARP2 levels were unchanged between normal and tumor tissues and few tumors showed overexpression of PARG (3.8%) or ARH3 (3.4%). Within the subgroup of triple negative tumors, PARG mRNA levels below the median were associated with a higher risk of developing metastases (p 5 0.039) raising the possibility this might be marker of clinical outcome.

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Poly(ADP-ribosyl)ation is implicated in the G0–G1 transition of resting cells

Cited by 34 publications

References 35 publications

QKI-Mediated Alternative Splicing of the Histone Variant MacroH2A1 Regulates Cancer Cell Proliferation

QKI-Mediated Alternative Splicing of the Histone Variant MacroH2A1 Regulates Cancer Cell Proliferation

Poly(ADP-ribose) polymerase 1 regulates nuclear reprogramming and promotes iPSC generation without c-Myc

Variations in the mRNA expression of poly(ADP‐ribose) polymerases, poly(ADP‐ribose) glycohydrolase and ADP‐ribosylhydrolase 3 in breast tumors and impact on clinical outcome

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