γ‐Tocopherol inhibits human cancer cell cycle progression and cell proliferation by down‐regulation of cyclins

2002 ◽  
Vol 16 (14) ◽  
pp. 1952-1954 ◽  
Author(s):  
René Gysin ◽  
Angelo Azzi ◽  
Theresa Visarius
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
Human Cancer Cell ◽  
Down Regulation ◽  
Cycle Progression

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.

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

Effects of 15-deoxy-Δ12, 14 prostaglandin J2 and ciglitazone on human cancer cell cycle progression and death: The role of PPARγ

2008 ◽  
Vol 580 (1-2) ◽  
pp. 80-86 ◽  
Author(s):  
Valéria Ferreira-Silva ◽  
Alice Cristina Rodrigues ◽  
Thiago Dominguez Crespo Hirata ◽  
Sandro Massao Hirabara ◽  
Rui Curi
Keyword(s):  
Cell Cycle ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
Human Cancer Cell ◽  
Cycle Progression ◽  
Prostaglandin J2

scholarly journals Effect of lycopene on cell viability and cell cycle progression in human cancer cell lines

2012 ◽  
Vol 12 (1) ◽  
pp. 36 ◽  
Author(s):  
Anderson Teodoro ◽  
Felipe Oliveira ◽  
Nathalia Martins ◽  
Guilherme de Maia ◽  
Renata Martucci ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cell Cycle Progression ◽  
Human Cancer ◽  
Cancer Cell Lines ◽  
Human Cancer Cell ◽  
Cycle Progression ◽  
Human Cancer Cell Lines

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.

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