CDK11p58 is required for the maintenance of sister chromatid cohesion

Hu, Dongli; Valentine, Marcus B.; Kidd, Vincent J.; Lahti, Jill M.

doi:10.1242/jcs.007963

Cited by 83 publications

(71 citation statements)

References 56 publications

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“…With a synchronized cell cycle, PTBP1-silenced cells were entered into the cell cycle in a rapid manner; however, the percentage of cells with an active cell cycle was low. Analysis on CDK11 p58 , critical regulator of cell mitosis (22), partially clarified this discrepancy. Reduced expression of PTBP1 downregulate CDK11 p58 , in turn, various cell-cycle mediators would be upregulated.…”

Section: Discussionmentioning

confidence: 99%

“…5A). For further analysis to explain the prolonged G 2 -M in HCT116 siPTBP1 cells, we performed immunoblotting of wholecell lysate for CDK11 p58 that is reported to play an important role for maintenance of sister chromosome cohesion (22). As a result, in HCT116 and DLD1 cells, when silencing PTBP1, CDK11 p58 protein levels were downregulated (Fig.…”

Section: Ptbp1 Promotes Cell Proliferation In Vivo and In Vitromentioning

confidence: 99%

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Significance of Polypyrimidine Tract–Binding Protein 1 Expression in Colorectal Cancer

Takahashi

Nishimura

Kagawa

et al. 2015

Molecular Cancer Therapeutics

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Polypyrimidine tract-binding protein (PTBP1) is an RNAbinding protein with various molecular functions related to RNA metabolism and a major repressive regulator of alternative splicing, causing exon skipping in numerous alternatively spliced pre-mRNAs. Here, we have investigated the role of PTBP1 in colorectal cancer. PTBP1 expression levels were significantly overexpressed in cancerous tissues compared with corresponding normal mucosal tissues. We also observed that PTBP1 expression levels, c-MYC expression levels, and PKM2: PKM1 ratio were positively correlated in colorectal cancer specimens. Moreover, PTBP1 expression levels were positively correlated to poor prognosis and lymph node metastasis. In analyses of colorectal cancer cells using siRNA for PTBP1, we observed that PTBP1 affects cell invasion, which was partially correlated to CD44 splicing, and this correlation was also confirmed in clinical samples. PTBP1 expression also affected anchorage-independent growth in colorectal cancer cell lines. PTBP1 expression also affected cell proliferation. Using timelapse imaging analysis, PTBP1 was implicated in prolonged G 2 -M phase in HCT116 cells. As for the mechanism of prolonged G 2 -M phase in HCT116 siPTBP1 cells, Western blotting revealed that PTBP1 expression level was correlated to CDK11 p58 expression level, which was reported to play an important role on progression to complete mitosis. These findings indicated that PTBP1 is a potential therapeutic target for colorectal cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Ptbp1 Promotes Cell Proliferation In Vivo and In Vitromentioning

confidence: 99%

Significance of Polypyrimidine Tract–Binding Protein 1 Expression in Colorectal Cancer

Takahashi

Nishimura

Kagawa

et al. 2015

Molecular Cancer Therapeutics

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“…[14][15][16][17][18][19] It is important therefore not to simply focus on how CDK11 regulates components of the autophagy machinery to bring about the effects we report knocked down by siRNA (Fig. 3A).…”

Section: Pitslre Is a Modulator Of Autophagymentioning

confidence: 99%

“…13 Subsequent studies on PITSLRE/CDK11 have revealed diverse roles for the kinase in controlling RNA splicing, apoptosis, sister chromatid adhesion and cytokinesis. [14][15][16][17][18][19] We add to these roles by showing that CDK11 is a fundamental regulator of autophagy. We show that while CDK11 appears to act as a turnover.…”

Section: Introductionmentioning

confidence: 99%

The cyclin-dependent kinase PITSLRE/CDK11 is required for successful autophagy

Wilkinson¹,

Croft²,

O’Prey³

et al. 2011

Autophagy

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(Macro)autophagy is a membrane-trafficking process that serves to sequester cellular constituents in organelles termed autophagosomes, which target their degradation in the lysosome. Autophagy operates at basal levels in all cells where it serves as a homeostatic mechanism to maintain cellular integrity. The levels and cargoes of autophagy can, however, change in response to a variety of stimuli, and perturbations in autophagy are known to be involved in the aetiology of various human diseases. Autophagy must therefore be tightly controlled. We report here that the Drosophila cyclin-dependent kinase PITSLRE is a modulator of autophagy. Loss of the human PITSLRE orthologue, CDK11, initially appears to induce autophagy, but at later time points CDK11 is critically required for autophagic flux and cargo digestion. Since PITSLRE/CDK11 regulates autophagy in both Drosophila and human cells, this kinase represents a novel phylogenetically conserved component of the autophagy machinery

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“…The second group of proteins belonging to Cdk family  Cdk7 to Cdk13  are involved in the activation of cell cycle kinases and transcriptional regulation (Akoulitchev et al, 2000;Chen et al, 2006;Chen et al, 2007;Garriga & Grana, 2004;Hu et al, 2007;Kasten & Giordano, 2001). Cdk7 in complex with Cyclin H is given a special importance since it is the only Cdk activating kinase (CAK) in mammalian cells phosphorylating a threonine residue in the conserved T-loop of Cdk (Lolli & Johnson, 2005).…”

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confidence: 99%