scholarly journals Targeting Abnormal Cell Cycle in Cancer: A Preface to the Special Issue

Onco ◽  
2022 ◽  
Vol 2 (1) ◽  
pp. 34-35
Author(s):  
Chiaki Takahashi ◽  
Jun-ya Kato
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
Special Issue ◽  
Cycle Progression ◽  
Abnormal Cell

The accelerated cell cycle progression is one of the hallmarks of human cancer [...]

scholarly journals Fbxl8 suppresses lymphoma growth and hematopoietic transformation through degradation of cyclin D3

Oncogene ◽  
2020 ◽  
Author(s):  
Akihiro Yoshida ◽  
Jaewoo Choi ◽  
Hong Ri Jin ◽  
Yan Li ◽  
Sagar Bajpai ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
E3 Ligase ◽  
Protein Stabilization ◽  
Cyclin D3 ◽  
Deficient Mutant ◽  
Cycle Progression ◽  
Functional Investigation

Abstract Overexpression of D-type cyclins in human cancer frequently occurs as a result of protein stabilization, emphasizing the importance of identification of the machinery that regulates their ubiqutin-dependent degradation. Cyclin D3 is overexpressed in ~50% of Burkitt’s lymphoma correlating with a mutation of Thr-283. However, the E3 ligase that regulates phosphorylated cyclin D3 and whether a stabilized, phosphorylation deficient mutant of cyclin D3, has oncogenic activity are undefined. We describe the identification of SCF-Fbxl8 as the E3 ligase for Thr-283 phosphorylated cyclin D3. SCF-Fbxl8 poly-ubiquitylates p-Thr-283 cyclin D3 targeting it to the proteasome. Functional investigation demonstrates that Fbxl8 antagonizes cell cycle progression, hematopoietic cell proliferation, and oncogene-induced transformation through degradation of cyclin D3, which is abolished by expression of cyclin D3T283A, a non-phosphorylatable mutant. Clinically, the expression of cyclin D3 is inversely correlated with the expression of Fbxl8 in lymphomas from human patients implicating Fbxl8 functions as a tumor suppressor.

scholarly journals CIP2A Modulates Cell-Cycle Progression in Human Cancer Cells by Regulating the Stability and Activity of Plk1

2013 ◽  
Vol 73 (22) ◽  
pp. 6667-6678 ◽  
Author(s):  
Jae-Sung Kim ◽  
Eun Ju Kim ◽  
Jeong Su Oh ◽  
In-Chul Park ◽  
Sang-Gu Hwang
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
Cycle Progression ◽  
Human Cancer Cells ◽  
The Stability

scholarly journals A Role for Homologous Recombination and Abnormal Cell-Cycle Progression in Radioresistance of Glioma-Initiating Cells

2012 ◽  
Vol 11 (9) ◽  
pp. 1863-1872 ◽  
Author(s):  
Yi Chieh Lim ◽  
Tara L. Roberts ◽  
Bryan W. Day ◽  
Angus Harding ◽  
Sergei Kozlov ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Homologous Recombination ◽  
Cell Cycle Progression ◽  
Cycle Progression ◽  
Abnormal Cell ◽  
Glioma Initiating Cells

scholarly journals LncRNA EPIC1 Promotes Cancer Cell Proliferation and Inhibits Apoptosis in Gallbladder Cancer Interacting with lncRNA LET

2020 ◽  
Author(s):  
Changbo Fu ◽  
Lei Nie ◽  
Tao Yin ◽  
Xuan Xu ◽  
weijun lu
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Gallbladder Cancer ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
Cancer Cell Proliferation ◽  
Cycle Progression ◽  
Tumor Tissues ◽  
Proliferation And Apoptosis

Abstract Background: LncRNA EPIC1 is likely involved in human cancer by promoting cell cycle progression. Our study was carried out to investigate the involvement of EPIC1 in gallbladder cancer (GBC). Methods: Expression levels of EPIC1 in two types of tissues (GBC and paracancerous) and plasma were measured by performing qPCR. GBC-SD and SGC-996 cells were transfected with LET and EPIC1 expression vectors.Results: In the preset study we found that EPIC1 was upregulated in tumor tissues than in paracancerous tissues of GBC patients, and plasma levels of EPIC1 were significantly correlated with levels of EPIC1 in tumor tissues. LncRNA LET was downregulated in tumor tissues than in paracancerous tissues and was inversely correlated with EPIC1 in both tumor tissues and paracancerous tissues. Overexpression of EPIC1 led to downregulated LET, and LET overexpression also mediated the downregulation of EPIC1. EPIC1 led to accelerated GBC cell proliferation and inhibited apoptosis. Overexpression of LET played opposites roles. In addition, overexpression of LET also attenuated the effects of EPIC1 overexpression on cancer cell proliferation and apoptosis. Conclusion: Therefore, therefore, lncRNA EPIC1 may promote cancer cell proliferation and inhibit apoptosis in GBC by interacting with LET.

scholarly journals p50 mono-ubiquitination and interaction with BARD1 regulates cell cycle progression and maintains genome stability

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Longtao Wu ◽  
Clayton D. Crawley ◽  
Andrea Garofalo ◽  
Jackie W. Nichols ◽  
Paige-Ashley Campbell ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Genome Stability ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
S Phase ◽  
Post Translational Modification ◽  
Chromosomal Breakage ◽  
Cycle Progression ◽  
Genome Wide ◽  
Phase Progression

Abstract p50, the mature product of NFKB1, is constitutively produced from its precursor, p105. Here, we identify BARD1 as a p50-interacting factor. p50 directly associates with the BARD1 BRCT domains via a C-terminal phospho-serine motif. This interaction is induced by ATR and results in mono-ubiquitination of p50 by the BARD1/BRCA1 complex. During the cell cycle, p50 is mono-ubiquitinated in S phase and loss of this post-translational modification increases S phase progression and chromosomal breakage. Genome-wide studies reveal a substantial decrease in p50 chromatin enrichment in S phase and Cycln E is identified as a factor regulated by p50 during the G1 to S transition. Functionally, interaction with BARD1 promotes p50 protein stability and consistent with this, in human cancer specimens, low nuclear BARD1 protein strongly correlates with low nuclear p50. These data indicate that p50 mono-ubiquitination by BARD1/BRCA1 during the cell cycle regulates S phase progression to maintain genome integrity.

Effect of N-acetyl cysteine on cell cycle progression of human cancer cell line

2000 ◽  
Vol 118 (4) ◽  
pp. A522
Author(s):  
Chikara Kusano ◽  
Sonshin Takao ◽  
Takashi Aikou ◽  
Hidezou Noma ◽  
Hiroyoshi Yoh ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Line ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
Cancer Cell Line ◽  
Human Cancer Cell Line ◽  
Human Cancer Cell ◽  
Cycle Progression ◽  
Acetyl Cysteine
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