NF-Y binds to both G1- and G2-specific cyclin promoters; a possible role in linking CDK2/Cyclin A to CDK1/Cyclin B

Chae, Hee-Don; Kim, Jungbin; Shin, Deug Y.

doi:10.5483/bmbrep.2011.44.8.553

Cited by 21 publications

(20 citation statements)

References 25 publications

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“…And while transcriptional activation of CHR-regulated genes has been shown to require binding of the heterotrimer NF-Y transcription factor (5,14,15), there was no significant difference in NF-YA occupancy at the cyclin B1 gene promoter in MVM-infected cells compared to that in doxorubicintreated or mock-treated cells (Fig. 4A).…”

Section: Figmentioning

confidence: 92%

“…It has at least five transcriptional promoter elements that regulate its expression. These include CCAAT boxes, GC boxes, E boxes, p53-responsive elements, and the cell cycle gene homology region (CHR), which bind NF-Y, SP1, Myc, p53, and the Myb-MuvB (MMB) complex, respectively (5)(6)(7)(8)(9)(10)(11)(12)(13). The CHR and its protein binding partners are important contributors to the intricate regulation of the cyclin B1 gene (14).…”

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confidence: 99%

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Minute Virus of Mice Inhibits Transcription of the Cyclin B1 Gene during Infection

Fuller

Majumder

Pintel

2017

J Virol

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Replication of minute virus of mice (MVM) induces a sustained cellular DNA damage response (DDR) which the virus then exploits to prepare the nuclear environment for effective parvovirus takeover. An essential aspect of the MVMinduced DDR is the establishment of a potent premitotic block, which we previously found to be independent of activated p21 and ATR/Chk1 signaling. This arrest, unlike others reported previously, depends upon a significant, specific depletion of cyclin B1 and its encoding RNA, which precludes cyclin B1/CDK1 complex function, thus preventing mitotic entry. We show here that while the stability of cyclin B1 RNA was not affected by MVM infection, the production of nascent cyclin B1 RNA was substantially diminished at late times postinfection. Ectopic expression of NS1 alone did not reduce cyclin B1 expression. MVM infection also reduced the levels of cyclin B1 protein, and RNA levels normally increased in response to DNA-damaging reagents. We demonstrated that at times of reduced cyclin B1 expression during infection, there was a significantly reduced occupancy of RNA polymerase II and the essential mitotic transcription factor FoxM1 on the cyclin B1 gene promoter. Additionally, while total FoxM1 levels remained constant, there was a significant decrease of the phosphorylated, likely active, forms of FoxM1. Targeting of a constitutively active FoxM1 construct or the activation domain of FoxM1 to the cyclin B1 gene promoter via clustered regularly interspaced short palindromic repeats (CRISPR)-enzymatically inactive Cas9 in MVM-infected cells increased both cyclin B1 protein and RNA levels, implicating FoxM1 as a critical target for cyclin B1 inhibition during MVM infection.IMPORTANCE Replication of the parvovirus minute virus of mice (MVM) induces a sustained cellular DNA damage response (DDR) which the virus exploits to prepare the nuclear environment for effective takeover. An essential aspect of the MVM-induced DDR is establishment of a potent premitotic block. This block depends upon a significant, specific depletion of cyclin B1 and its encoding RNA that precludes cyclin B1/CDK1 complex functions necessary for mitotic entry. We show that reduced cyclin B1 expression is controlled primarily at the level of transcription initiation. Additionally, the essential mitotic transcription factor FoxM1 and RNA polymerase II were found to occupy the cyclin B1 gene promoter at reduced levels during infection. Recruiting a constitutively active FoxM1 construct or the activation domain of FoxM1 to the cyclin B1 gene promoter via CRISPR-catalytically inactive Cas9 (dCas9) in MVM-infected cells increased expression of both cyclin B1 protein and RNA, implicating FoxM1 as a critical target mediating MVM-induced cyclin B1 inhibition.

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Section: Figmentioning

confidence: 92%

mentioning

confidence: 99%

Minute Virus of Mice Inhibits Transcription of the Cyclin B1 Gene during Infection

Fuller

Majumder

Pintel

2017

J Virol

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“…The orderly progression of the cell cycle is affected through the periodic activation and inactivation of a series of CDKs (37). G1/S checkpoints are located at the end of the G1 phase of the cell cycle, just before entry into the S phase.…”

Section: Discussionmentioning

confidence: 99%

Nitidine chloride inhibits hepatocellular carcinoma cell growth in vivo through the suppression of the JAK1/STAT3 signaling pathway

Liao

Zheng

et al. 2013

International Journal of Molecular Medicine

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Abstract. Signal transducer and activator of transcription 3 (STAT3) is persistently activated in cancer cells and contributes to malignant progression in various types of cancer. The Janus-activated kinase (JAK) family phosphorylates STAT3 in response to stimulation by cytokines or growth factors. The JAK1-STAT3 signaling pathway plays an important role in cell proliferation and apoptosis. Nitidine chloride (NC) is a benzophenanthridine alkaloid that has been reported as an antitumor agent due to its its inhibitory effects on topoisomerase I. Using a mouse xenograft model of hepatocellular carcinoma (HCC), this study aimed to evaluate the effects of NC on tumor growth in vivo and to elucidate the underlying mechanisms. The analysis of the effects of NC on apoptosis in HCC tumor xenografts in mice was carried out by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay; the expression of Bcl-2, Bax, cyclin-dependent kinase (CDK)4, cyclin D1, p21 and proliferating cell nuclear antigen (PCNA) was analyzed by immunohistochemistry; and the protein expression of JAK1 and STAT3 was examined by western blot analysis. Our results revealed that treatment with NC decreased the tumor volume and tumor weight, suggesting that NC inhibits HCC cell growth in vivo. In addition, NC blocked the activation of JAK1-STAT3 in the tumor tissues, which in turn resulted in the induction of cancer cell apoptosis and the inhibition of proliferation. Consequently, treatment with NC downregulated the expression of cyclin D1, CDK4 and Bcl-2 and increased the level of p21 and Bax. Our data provide a molecular basis for the antitumor activity of NC. IntroductionHepatocellular carcinoma (HCC) is the third leading cause of cancer-related mortality worldwide (1,2) and it has been reported that more than 600,000 individuals succumb to the disease each year (1). It is the second most common cause of cancer-related mortality in China, and 75% of known new cases and deaths in the Asia-Pacific region (3-5). Currently, the main treatment methods for liver cancer include surgical resection, radiotherapy and chemotherapy (4,6). Although surgical resection (which involves removing the tumor completely) offers the best prognosis for long-term survival, only 10-15% of patients are suitable for surgical resection, as the tumor may be too large, or may have grown into major blood vessels or other vital organs (7-9). Related data demonstrate that the percentage of HCC cells is already high at diagnosis with a high expression of the multidrug resistance gene and conventional chemotherapy of HCC fails to provide satisfactory remission and may cause serious side-effects (6,10). Thus, it is necessary to develop a novel effective drug for the treatment of HCC. Natural products have attracted much attention in the search for novel anticancer therapeutic agents as they have relatively few side-effects and have long been used as alternative therapies for various diseases, including cancer (11,12). Therefore, determining naturally occurrin...

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“…Moreover, it also binds to and activates cdk1, a kinase necessary for G 2 /M transition (1). The role of cyclin A-cdk complexes during cell cycle is to phosphorylate a plethora of substrates that include a significant number of transcription factors as for instance Sp1, NF-Y, FOXK2, and PR (2)(3)(4)(5), transcriptional repressors as pRb and RBP1 (6), or proteins involved in epigenetic gene silencing as EZH2 (7). Thus cyclin A-cdk complexes play a crucial role in the regulation of gene expression during cell cycle progression.…”

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confidence: 99%

Histone Deacetylase 3 Regulates Cyclin A Stability

Vidal-Laliena

Gallastegui

Mateo

et al. 2013

Journal of Biological Chemistry

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NF-Y binds to both G1- and G2-specific cyclin promoters; a possible role in linking CDK2/Cyclin A to CDK1/Cyclin B

Cited by 21 publications

References 25 publications

Minute Virus of Mice Inhibits Transcription of the Cyclin B1 Gene during Infection

Minute Virus of Mice Inhibits Transcription of the Cyclin B1 Gene during Infection

Nitidine chloride inhibits hepatocellular carcinoma cell growth in vivo through the suppression of the JAK1/STAT3 signaling pathway

Histone Deacetylase 3 Regulates Cyclin A Stability

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