scholarly journals p300/CBP Methylation is Involved in the Potential Carcinogenic Mechanism of Lung Cancer

2021 ◽  
Author(s):  
Yu Zhang ◽  
Wei Shen ◽  
Jin Zou ◽  
Shibo Ying
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Transcription Factors ◽  
Structure Function ◽  
Histone Acetyltransferase ◽  
Specific Substrate ◽  
Wide Range ◽  
A Cell ◽  
Kix Domain ◽  
Pka Pathway

p300/CBP is involved in the expression of a wide range of genes, both as a histone acetyltransferase (HAT) and as a coactivator of transcription factors. p300/CBP is the specific substrate of CARM1, and its KIX domain and GBD domain are the main sites methylated by arginine methyltransferase 4 (PRMT4/CARM1). p300/CBP plays an important role in lung cancer, which is a cell cycle disease. More importantly, the methylation of p300/CBP by CARM1 affects the progression of lung cancer through the cAMP-PKA pathway, p53 pathway and ER pathway. The structure, function, methylation modification sites, methylation-related enzymes, genes associated with lung cancer and the possible mechanisms of p300/CBP action are reviewed.

Validation of a cell cycle progression score for 5-year mortality risk in patients with stage I non-small cell lung cancer.

2015 ◽  
Vol 33 (15_suppl) ◽  
pp. 7522-7522
Author(s):  
Takashi Eguchi ◽  
Kadota Kyuichi ◽  
Brent Evans ◽  
Camelia S. Sima ◽  
Thaylon Davis ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Cycle ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Mortality Risk ◽  
Cell Cycle Progression ◽  
Small Cell ◽  
Small Cell Lung ◽  
Cycle Progression ◽  
A Cell

scholarly journals Synergy of Topoisomerase and Structural-Maintenance-of-Chromosomes Proteins Creates a Universal Pathway to Simplify Genome Topology

2018 ◽  
Author(s):  
Enzo Orlandini ◽  
Davide Marenduzzo ◽  
Davide Michieletto
Keyword(s):  
Cell Cycle ◽  
Specific Substrate ◽  
Biological Processes ◽  
Type Ii ◽  
Synergistic Mechanism ◽  
A Cell ◽  
Structural Maintenance Of Chromosomes ◽  
Knots And Links ◽  
Smc Proteins

Topological entanglements severely interfere with important biological processes. For this reason, genomes must be kept unknotted and unlinked during most of a cell cycle. Type II Topoisomerase (TopoII) enzymes play an important role in this process but the precise mechanisms yielding systematic disentanglement of DNA in vivo are not clear. Here we report computational evidence that Structural Maintenance of Chromosomes (SMC) proteins – such as cohesins and condensins – can cooperate with TopoII to establish a synergistic mechanism to resolve topological entanglements. SMC-driven loop extrusion (or diffusion) induces the spatial localisation of essential crossings in turn catalysing the simplification of knots and links by TopoII enzymes even in crowded and confined conditions. The mechanism we uncover is universal in that it does not qualitatively depend on the specific substrate, whether DNA or chromatin, or on SMC processivity; we thus argue that this synergy may be at work across organisms and throughout the cell cycle.

p53 functions as a cell cycle control protein in osteosarcomas

1990 ◽  
Vol 10 (11) ◽  
pp. 5772-5781
Author(s):  
L Diller ◽  
J Kassel ◽  
C E Nelson ◽  
M A Gryka ◽  
G Litwak ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Control ◽  
P53 Gene ◽  
Tumor Formation ◽  
Wild Type ◽  
Gene Encoding ◽  
Wide Range ◽  
A Cell ◽  
Wild Type P53

Mutations in the p53 gene have been associated with a wide range of human tumors, including osteosarcomas. Although it has been shown that wild-type p53 can block the ability of E1a and ras to cotransform primary rodent cells, it is poorly understood why inactivation of the p53 gene is important for tumor formation. We show that overexpression of the gene encoding wild-type p53 blocks the growth of osteosarcoma cells. The growth arrest was determined to be due to an inability of the transfected cells to progress into S phase. This suggests that the role of the p53 gene as an antioncogene may be in controlling the cell cycle in a fashion analogous to the check-point control genes in Saccharomyces cerevisiae.

scholarly journals 14-3-3 proteins: a family of versatile molecular regulators

2008 ◽  
pp. S11-S21
Author(s):  
V Obšilová ◽  
J Šilhan ◽  
E Bouřa ◽  
J Teisinger ◽  
T Obšil
Keyword(s):  
Cell Cycle ◽  
Transcription Factors ◽  
Cell Cycle Regulation ◽  
Molecular Scaffolds ◽  
Forkhead Transcription Factors ◽  
Binding Partners ◽  
Wide Range ◽  
Functional Modulation ◽  
Cycle Regulation ◽  
And Control

The 14-3-3 proteins are a family of acidic regulatory molecules found in all eukaryotes. 14-3-3 proteins function as molecular scaffolds by modulating the conformation of their binding partners. Through the functional modulation of a wide range of binding partners, 14-3-3 proteins are involved in many processes, including cell cycle regulation, metabolism control, apoptosis, and control of gene transcription. This minireview includes a short overview of 14-3-3 proteins and then focuses on their role in the regulation of two important binding partners: FOXO forkhead transcription factors and an enzyme tyrosine hydroxylase.

scholarly journals In vitro cell cycle oscillations exhibit a robust and hysteretic response to changes in cytoplasmic density

2021 ◽  
Author(s):  
Minjun Jin ◽  
Franco Tavella ◽  
Shiyuan Wang ◽  
Qiong Yang
Keyword(s):  
Cell Cycle ◽  
Oscillatory Behavior ◽  
Cycle Number ◽  
Biochemical Processes ◽  
Cellular Processes ◽  
Wide Range ◽  
A Cell ◽  
Xenopus Egg ◽  
Number Of Cycles

Cells control the properties of the cytoplasm to ensure the proper functioning of biochemical processes. Recent studies showed that the density of the cytoplasm varies in both physiological and pathological states of cells undergoing growth, division, differentiation, apoptosis, senescence, and metabolic starvation. Little is known about how cellular processes cope with these cytoplasmic variations. Here we study how a cell cycle oscillator comprising cyclin-dependent kinase (CDK1) responds to cytoplasmic density changes by systematically diluting or concentrating a cycling Xenopus egg cytoplasm in cell-like microfluidic droplets. We found that the cell cycle maintains robust oscillations over a wide range of deviations from the endogenous density by as low as 0.2x to more than 1.22x. A further dilution or concentration from these values will arrest the system in a low or high steady-state of CDK1 activity, respectively. Interestingly, diluting a concentrated arrested cytoplasm recovers its oscillatory behavior but requires a significantly lower concentration than 1.22x. Thus, the cell cycle switches reversibly between oscillatory and stable steady states at distinct thresholds depending on the direction of density tuning, forming a hysteresis loop. We recapitulated these observations by a mathematical model. The model predicted that Wee1 and Cdc25 positive feedback do not contribute to the observed robustness, confirmed by experiments. Nevertheless, modulating these feedback strengths and cytoplasmic density changes the total number of cycles, revealing a new role of Wee1 and Cdc25 in controlling the cycle number of early embryonic extracts. Our system can be applied to study how cytoplasmic density affects other cellular processes.

scholarly journals Palbociclib-mediated cell cycle arrest can occur in the absence of the CDK inhibitors p21 and p27

Open Biology ◽  
2021 ◽  
Vol 11 (11) ◽  
Author(s):  
Betheney R. Pennycook ◽  
Alexis R. Barr
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Mechanism Of Action ◽  
Quantitative Imaging ◽  
Cancer Therapies ◽  
Cycle Arrest ◽  
Wide Range ◽  
Cast Doubt ◽  
A Cell ◽  
G1 Cell Cycle Arrest

The use of CDK4/6 inhibitors in the treatment of a wide range of cancers is an area of ongoing investigation. Despite their increasing clinical use, there is limited understanding of the determinants of sensitivity and resistance to these drugs. Recent data have cast doubt on how CDK4/6 inhibitors arrest proliferation, provoking renewed interest in the role(s) of CDK4/6 in driving cell proliferation. As the use of CDK4/6 inhibitors in cancer therapies becomes more prominent, an understanding of their effect on the cell cycle becomes more urgent. Here, we investigate the mechanism of action of CDK4/6 inhibitors in promoting cell cycle arrest. Two main models explain how CDK4/6 inhibitors cause G1 cell cycle arrest, which differ in their dependence on the CDK inhibitor proteins p21 and p27. We have used live and fixed single-cell quantitative imaging, with inducible degradation systems, to address the roles of p21 and p27 in the mechanism of action of CDK4/6 inhibitors. We find that CDK4/6 inhibitors can initiate and maintain a cell cycle arrest without p21 or p27. This work clarifies our current understanding of the mechanism of action of CDK4/6 inhibitors and has implications for cancer treatment and patient stratification.

scholarly journals p53 functions as a cell cycle control protein in osteosarcomas.

1990 ◽  
Vol 10 (11) ◽  
pp. 5772-5781 ◽  
Author(s):  
L Diller ◽  
J Kassel ◽  
C E Nelson ◽  
M A Gryka ◽  
G Litwak ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Control ◽  
P53 Gene ◽  
Tumor Formation ◽  
Wild Type ◽  
Gene Encoding ◽  
Wide Range ◽  
A Cell ◽  
Wild Type P53

Mutations in the p53 gene have been associated with a wide range of human tumors, including osteosarcomas. Although it has been shown that wild-type p53 can block the ability of E1a and ras to cotransform primary rodent cells, it is poorly understood why inactivation of the p53 gene is important for tumor formation. We show that overexpression of the gene encoding wild-type p53 blocks the growth of osteosarcoma cells. The growth arrest was determined to be due to an inability of the transfected cells to progress into S phase. This suggests that the role of the p53 gene as an antioncogene may be in controlling the cell cycle in a fashion analogous to the check-point control genes in Saccharomyces cerevisiae.

scholarly journals Synergy of topoisomerase and structural-maintenance-of-chromosomes proteins creates a universal pathway to simplify genome topology

2019 ◽  
Vol 116 (17) ◽  
pp. 8149-8154 ◽  
Author(s):  
Enzo Orlandini ◽  
Davide Marenduzzo ◽  
Davide Michieletto
Keyword(s):  
Cell Cycle ◽  
Spatial Localization ◽  
Specific Substrate ◽  
Biological Processes ◽  
Type Ii ◽  
Synergistic Mechanism ◽  
A Cell ◽  
Structural Maintenance Of Chromosomes ◽  
Knots And Links

Topological entanglements severely interfere with important biological processes. For this reason, genomes must be kept unknotted and unlinked during most of a cell cycle. Type II topoisomerase (TopoII) enzymes play an important role in this process but the precise mechanisms yielding systematic disentanglement of DNA in vivo are not clear. Here we report computational evidence that structural-maintenance-of-chromosomes (SMC) proteins—such as cohesins and condensins—can cooperate with TopoII to establish a synergistic mechanism to resolve topological entanglements. SMC-driven loop extrusion (or diffusion) induces the spatial localization of essential crossings, in turn catalyzing the simplification of knots and links by TopoII enzymes even in crowded and confined conditions. The mechanism we uncover is universal in that it does not qualitatively depend on the specific substrate, whether DNA or chromatin, or on SMC processivity; we thus argue that this synergy may be at work across organisms and throughout the cell cycle.

scholarly journals Palbociclib-mediated cell cycle arrest can occur in the absence of the CDK inhibitors p21 and p27

2021 ◽  
Author(s):  
Betheney R Pennycook ◽  
Alexis R Barr
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Mechanism Of Action ◽  
Quantitative Imaging ◽  
Cancer Therapies ◽  
Cycle Arrest ◽  
Wide Range ◽  
Cast Doubt ◽  
A Cell ◽  
G1 Cell Cycle Arrest

The use of CDK4/6 inhibitors in the treatment of a wide range of cancers is an area of ongoing investigation. Despite their increasing clinical use, there is limited understanding of the determinants of sensitivity and resistance to these drugs. Recent data has cast doubt on how CDK4/6 inhibitors arrest proliferation, provoking renewed interest in the role(s) of CDK4/6 in driving cell proliferation. As the use of CDK4/6 inhibitors in cancer therapies becomes more prominent, an understanding of their effect on the cell cycle becomes more urgent. Here, we investigate the mechanism of action of CDK4/6 inhibitors in promoting cell cycle arrest. Two main models explain how CDK4/6 inhibitors cause G1 cell cycle arrest, which differ in their dependence on the CDK inhibitor proteins p21 and p27. We have used live and fixed single-cell quantitative imaging, with inducible degradation systems, to address the roles of p21 and p27 in the mechanism of action of CDK4/6 inhibitors. We find that CDK4/6 inhibitors can initiate and maintain a cell cycle arrest without p21 or p27. This work clarifies our current understanding of the mechanism of action of CDK4/6 inhibitors and has implications for cancer treatment and patient stratification.

357: Interstitial Cystitis Anti-Proliferative Factor (APF) as a Cell-Cycle Modulator

2004 ◽  
Vol 171 (4S) ◽  
pp. 93-94
Author(s):  
Hani Rashid ◽  
Susan Keay ◽  
Chen-Ou Zhang ◽  
Edward M. Messing ◽  
Jay Reeder
Keyword(s):  
Cell Cycle ◽  
Interstitial Cystitis ◽  
A Cell
Sign in / Sign up

Export Citation Format

Share Document