Inhibition of ultraviolet B (UVB) induced apoptosis in A431 cells by mimosine is not dependent on cell cycle arrest

2002 ◽  
Vol 80 (7) ◽  
pp. 650-653
Author(s):  
D O Cliche ◽  
S Girouard ◽  
N Bissonnette ◽  
D J Hunting
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Rna Polymerase Ii ◽  
Ultraviolet B ◽  
Caspase Activation ◽  
A431 Cells ◽  
Cycle Arrest ◽  
Activation Assay ◽  
G1 Cell Cycle Arrest ◽  
Induced Apoptosis

Ultraviolet (UV) radiation is a strong apoptotic trigger in many cell types. We have previously reported that a plant amino acid, mimosine (beta-[N-(3-hydroxy-4-pyridone)]-alpha-aminopropionic acid), with a well-known reversible G1 cell cycle arrest activity can inhibit apoptosis induced by UV irradiation and RNA polymerase II blockage in human A431 cells. Here, apoptosis was measured with a fluorimetric caspase activation assay. Interestingly, the protective state was effective up to 24 h following removal of mimosine from the culture medium while cells were progressing in the cell cycle. Our results demonstrate that the protective effect of mimosine against UV-induced apoptosis can be dissociated from its G1 cell-cycle arrest activity.Key words: mimosine, apoptosis, cell cycle, A431 cells, caspase activation assay.

Honokiol, a chemopreventive agent against skin cancer, induces cell cycle arrest and apoptosis in human epidermoid A431 cells

2011 ◽  
Vol 236 (11) ◽  
pp. 1351-1359 ◽  
Author(s):  
Chandeshwari Chilampalli ◽  
Ruth Guillermo ◽  
Radhey S Kaushik ◽  
Alan Young ◽  
Gudiseva Chandrasekher ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Skin Cancer ◽  
Cell Cycle Arrest ◽  
Squamous Carcinoma ◽  
Ultraviolet B ◽  
Dependent Manner ◽  
A431 Cells ◽  
Squamous Carcinoma Cells ◽  
Cycle Arrest ◽  
M Phase

Honokiol is a plant lignan isolated from bark and seed cones of Magnolia officinalis. Recent studies from our laboratory indicated that honokiol pretreatment decreased ultraviolet B-induced skin cancer development in SKH-1 mice. The aim of the present investigation was to study the effects of honokiol on human epidermoid squamous carcinoma A431 cells and to elucidate possible mechanisms involved in preventing skin cancer. A431 cells were pretreated with different concentrations of honokiol for a specific time period and investigated for effects on apoptosis and cell cycle analysis. Treatment with honokiol significantly decreased cell viability and cell proliferation in a concentration- and time-dependent manner. Honokiol pretreatment at 50 μmol/L concentration induced G0/G1 cell cycle arrest significantly ( P < 0.05) and decreased the percentage of cells in the S and G2/M phase. Honokiol down-regulated the expression of cyclin D1, cyclin D2, Cdk2, Cdk4 and Cdk6 proteins and up-regulated the expression of Cdk's inhibitor proteins p21 and p27. Pretreatment of A431 cells with honokiol leads to induction of apoptosis and DNA fragmentation. These findings indicate that honokiol provides its effects in squamous carcinoma cells by inducing cell cycle arrest at G0/G1 phase and apoptosis.

scholarly journals Loss of p21 disrupts p14ARF-induced G1 cell cycle arrest but augments p14ARF-induced apoptosis in human carcinoma cells

Oncogene ◽  
2005 ◽  
Vol 24 (25) ◽  
pp. 4114-4128 ◽  
Author(s):  
Philipp G Hemmati ◽  
Guillaume Normand ◽  
Berlinda Verdoodt ◽  
Clarissa von Haefen ◽  
Anne Hasenjäger ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Human Carcinoma ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
Induced Apoptosis

scholarly journals G1 Cell Cycle Arrest and Extrinsic Apoptotic Mechanisms Underlying the Anti-Leukemic Activity of CDK7 Inhibitor BS-181

Cancers ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3845
Author(s):  
Shin Young Park ◽  
Ki Yun Kim ◽  
Do Youn Jun ◽  
Su-Kyeong Hwang ◽  
Young Ho Kim
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Jurkat Cells ◽  
Parp Cleavage ◽  
Caspase 8 ◽  
Down Regulation ◽  
Blocking Antibody ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
Induced Apoptosis

In vitro antitumor activity of the CDK7 inhibitor BS-181 against human T-ALL Jurkat cells was determined. Treatment of Jurkat clones (JT/Neo) with BS-181 caused cytotoxicity and several apoptotic events, including TRAIL/DR4/DR5 upregulation, c-FLIP down-regulation, BID cleavage, BAK activation, ΔΨm loss, caspase-8/9/3 activation, and PARP cleavage. However, the BCL-2-overexpressing Jurkat clone (JT/BCL-2) abrogated these apoptotic responses. CDK7 catalyzed the activating phosphorylation of CDK1 (Thr161) and CDK2 (Thr160), and CDK-directed retinoblastoma phosphorylation was attenuated in both BS-181-treated Jurkat clones, whereas only JT/BCL-2 cells exhibited G1 cell cycle arrest. The G1-blocker hydroxyurea augmented BS-181-induced apoptosis by enhancing TRAIL/DR4/DR5 upregulation and c-FLIP down-regulation. BS-181-induced FITC–annexin V-positive apoptotic cells were mostly in the sub-G1 and G1 phases. BS-181-induced cytotoxicity and mitochondrial apoptotic events (BAK activation/ΔΨm loss/caspase-9 activation) in Jurkat clones I2.1 (FADD-deficient) and I9.2 (caspase-8-deficient) were significantly lower than in A3 (wild-type). Exogenously added recombinant TRAIL (rTRAIL) markedly synergized BS-181-induced apoptosis in A3 cells but not in normal peripheral T cells. The cotreatment cytotoxicity was significantly reduced by the DR5-blocking antibody but not by the DR4-blocking antibody. These results demonstrated that the BS-181 anti-leukemic activity is attributed to extrinsic TRAIL/DR5-dependent apoptosis preferentially induced in G1-arrested cells, and that BS-181 and rTRAIL in combination may hold promise for T-ALL treatment.

Loss of p21 disrupts p14ARF-induced G1 cell cycle arrest but augments p14ARF induced apoptosis in human carcinoma cells

2005 ◽  
Vol 2005 (Fall) ◽  
Author(s):  
Philipp G. Hemmati ◽  
Guillaume Normand ◽  
Bernd Gillissen ◽  
Clarissa von Haefen ◽  
Jana Wendt ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Carcinoma Cells ◽  
Human Carcinoma ◽  
Cycle Arrest ◽  
G1 Cell Cycle Arrest ◽  
Induced Apoptosis

Nickel(II) bis(isatin thiosemicarbazone) complexes induced apoptosis through mitochondrial signaling pathway and G0/G1 cell cycle arrest in IM-9 cells

2018 ◽  
Vol 182 ◽  
pp. 208-221 ◽  
Author(s):  
Chandrasekar Balachandran ◽  
Jebiti Haribabu ◽  
Kumaramangalam Jeyalakshmi ◽  
Nattamai S.P. Bhuvanesh ◽  
Ramasamy Karvembu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
Cycle Arrest ◽  
Mitochondrial Signaling ◽  
Thiosemicarbazone Complexes ◽  
G1 Cell Cycle Arrest ◽  
Induced Apoptosis
Sign in / Sign up

Export Citation Format

Share Document