Control of CCND1 ubiquitylation by the catalytic SAGA subunit USP22 is essential for cell cycle progression through G1 in cancer cells

Gennaro, Victoria; Stanek, Timothy J.; Peck, Amy R.; Sun, Yunguang; Wang, Feng; Qie, Shuo; Knudsen, Karen E.; Rui, Hallgeir; Butt, Tauseef R.; Diehl, J. Alan; McMahon, Steven B.

doi:10.1073/pnas.1807704115

Cited by 101 publications

(89 citation statements)

References 70 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Usp22 depletion in cultured cells has been associated with G1/M cell cycle arrest (Gennaro et al, 2018;Zhang et al, 2008b), proliferation defects (Atanassov and Dent, 2011), p53-dependent apoptosis (Lin et al, 2012) and blockage of stem cell differentiation (Sussman et al, 2013). Although no defects in proliferation or increased cell death were observed at E9.5 ( Fig.…”

Section: Introductionmentioning

confidence: 95%

“…Unfortunately, studies to date have yielded a confusing amalgam of possible roles for USP22 in oncogenesis. Several studies have focused on potential roles for USP22 in regulating cell cycle progression through effects on oncogenes such as BMI1 (Liu et al, 2012), c-MYC (MYC) (Zhang et al, 2008a), SIRT1 (Lin et al, 2012), cyclin B1 (Lin et al, 2015), cyclin D1 (Gennaro et al, 2018) and KDM1A (Zhou et al, 2016), or on tumor suppressors such as p53 (Trp53) (Ding et al, 2015;Lin et al, 2012;Lv et al, 2011). The previously defined 11-gene 'death from cancer' signature that includes USP22 also includes BMI1 and downstream targets of this polycomb group protein.…”

Section: Examination Of Monoubiquitination Of Histone H2b (H2bub1) Inmentioning

confidence: 99%

See 1 more Smart Citation

USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

et al. 2019

View full text Add to dashboard Cite

USP22, a component of the SAGA complex, is overexpressed in highly aggressive cancers, but the normal functions of this deubiquitinase are not well defined. We determined that loss of USP22 in mice results in embryonic lethality due to defects in extra-embryonic placental tissues and failure to establish proper vascular interactions with the maternal circulatory system. These phenotypes arise from abnormal gene expression patterns that reflect defective kinase signaling, including TGFβ and several receptor tyrosine kinase pathways. USP22 deletion in endothelial cells and pericytes that are induced from embryonic stem cells also hinders these signaling cascades, with detrimental effects on cell survival and differentiation as well as on the ability to form vessels. Our findings provide new insights into the functions of USP22 during development that may offer clues to its role in disease states.

show abstract

Section: Introductionmentioning

confidence: 95%

Section: Examination Of Monoubiquitination Of Histone H2b (H2bub1) Inmentioning

confidence: 99%

USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

et al. 2019

View full text Add to dashboard Cite

show abstract

“…Recently, several deubiquitinases have been reported to be involved in cell cycle progression. USP2 and USP22 can stabilize cyclin D1 to promote cell cycle progression [16,17]. A recent study also revealed that a small molecule, ML364, can inhibit USP2 to promote degradation, leading to cell cycle arrest [18].…”

Section: Usps Are Involved In Cell Cycle Progressionmentioning

confidence: 99%

The role of ubiquitin-specific peptidases in cancer progression

et al. 2019

View full text Add to dashboard Cite

Protein ubiquitination is an important mechanism for regulating the activity and levels of proteins under physiological conditions. Loss of regulation by protein ubiquitination leads to various diseases, such as cancer. Two types of enzymes, namely, E1/E2/E3 ligases and deubiquitinases, are responsible for controlling protein ubiquitination. The ubiquitin-specific peptidases (USPs) are the main members of the deubiquitinase family. Many studies have addressed the roles of USPs in various diseases. An increasing number of studies have indicated that USPs are critical for cancer progression, and some USPs have been used as targets to develop inhibitors for cancer prevention. Herein we collect and organize most of the recent studies on the roles of USPs in cancer progression and discuss the development of USP inhibitors for cancer therapy in the future.

show abstract

“…CCND1 has an A/G polymorphism at nucleotide 870, at the splice donor site of the exon 4-intron 4 boundary. This polymorphism leads to alternative splicing, generating a cyclin D1 variant called cyclin D1b [50] ( Figure 1B). The mature cyclin D1b transcript includes exon 4 and intron 4.…”

Section: Cyclin D1 Accumulates In the Nucleus And/or In The Cytoplasmmentioning

confidence: 99%

The double dealing of cyclin D1

2019

View full text Add to dashboard Cite

Abbreviations: aa, amino acid ; AR, androgen receptor; ATM, ataxia telangectasia mutant;ATR, ATM and Rad3-related; CDK, cyclin-dependent kinase; ChREBP, carbohydrate response element binding protein; CIP, CDK-interacting protein; CHK1/2, checkpoint kinase 1/2; CKI, CDK inhibitor; DDR, DNA damage response; DMP1, cyclin D-binding myb-like protein; DSB, double-strand DNA break; DNA-PK, DNA-dependent protein kinase; ER, estrogen receptor; FASN, fatty acid synthase; GSK3β, glycogen synthase-3β; HAT, histone acetyltransferase; HDAC, histone deacetylase; HK2, hexokinase 2; HNF4α, and hepatocyte nuclear factor 4α; HR, homologous recombination; IR, ionizing radiation; KIP, kinase inhibitory protein; MCL, mantle cell lymphoma; NHEJ, non-homologous end-joining; PCAF, p300/CREB binding-associated protein; PGC1α, PPARγ co-activator 1α; PEST, proline-glutamic acid-serine-threonine, PK, pyruvate kinase; PPAR, peroxisome proliferator-activated receptor; RB1, retinoblastoma protein; ROS, reactive oxygen species; SRC, steroid receptor coactivator; STAT, signal transducer and activator of transcription; TGFβ, transforming growth factor β; UPS, ubiquitinproteasome system; USP22, ubiquitin-specific peptidase 22; XPO1 (or CRM1) exportin 1. AbstractThe cell cycle is tightly regulated by cyclins and their catalytic moieties, the cyclindependent kinases (CDKs). Cyclin D1, in association with CDK4/6, acts as a mitogenic sensor and integrates extracellular mitogenic signals and cell cycle progression. When deregulated (overexpressed, accumulated, inappropriately located), cyclin D1 becomes an oncogene and is recognized as a driver of solid tumors and hemopathies. Recent studies on the oncogenic roles of cyclin D1 reported non-canonical functions dependent on the partners of cyclin D1 and its location within tumor cells or tissues. Support for these new functions was provided by various mouse models of oncogenesis. Finally, proteomic and transcriptomic data identified complex cyclin D1 networks. This review focuses on these aspects of cyclin D1 pathophysiology, which may be crucial for targeted therapy.

show abstract

Control of CCND1 ubiquitylation by the catalytic SAGA subunit USP22 is essential for cell cycle progression through G1 in cancer cells

Cited by 101 publications

References 70 publications

USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

USP22 controls multiple signaling pathways that are essential for vasculature formation in the mouse placenta

The role of ubiquitin-specific peptidases in cancer progression

The double dealing of cyclin D1

Contact Info

Product

Resources

About