Influence of co-exposure to methylparaben and dibutyl phthalate used in chemical/cosmetic industry on caspase-3/7 activity in A431 cells

2021 ◽  
Vol 350 ◽  
pp. S205-S206
Author(s):  
K. Miranowicz-Dzierżawska ◽  
L. Zapór ◽  
J. Skowroń ◽  
L. Chojnacka-Puchta ◽  
D. Sawicka
Keyword(s):  
Caspase 3 ◽  
Dibutyl Phthalate ◽  
A431 Cells ◽  
Cosmetic Industry

Apoptotic signalling cascade in photosensitized human epidermal carcinoma A431 cells: involvement of singlet oxygen, c-Jun N-terminal kinase, caspase-3 and p21-activated kinase 2

2000 ◽  
Vol 351 (1) ◽  
pp. 221-232 ◽  
Author(s):  
Wen-Hsiung CHAN ◽  
Jau-Song YU ◽  
Shiaw-Der YANG
Keyword(s):  
Singlet Oxygen ◽  
Caspase 3 ◽  
Early Stage ◽  
A431 Cells ◽  
Caspase Family ◽  
P21 Activated Kinase ◽  
Induced Apoptosis ◽  
Jnk Activation ◽  
Epidermal Carcinoma ◽  
Signalling Cascade

Photodynamic treatment (PDT) elicits diverse cellular responses and can also cause apoptosis. In the present study the cascade of signalling events involved in PDT-induced apoptosis was investigated using Rose Bengal (RB) as the photosensitizer, and human epidermal carcinoma A431 cells as the cell model. We show that a 36-kDa kinase detected by an in-gel kinase assay is markedly activated during PDT-triggered apoptosis. Immunoblot analysis revealed that this 36-kDa kinase represents the C-terminal catalytic fragment of p21-activated kinase (PAK)2. Generation of this active fragment of PAK2 is mediated by the caspase family of proteases, which are activated by PDT. The specific caspase inhibitors (acetyl-Asp-Glu-Val-Asp-aldehyde and acetyl-Tyr-Val-Ala-Asp-chloromethylketone) block the PDT-induced caspase-3 activation and subsequent PAK2 cleavage/activation, indicating a major role for the caspase family proteases in PDT-induced apoptosis. Both PDT-induced caspase-3 activation and PAK2 cleavage/activation can be inhibited by the singlet oxygen scavengers, L-histidine and α-tocopherol, but not the hydroxyl radical scavenger, mannitol, demonstrating that singlet oxygen is an immediate early-apoptotic signal generated by PDT. In addition, PDT can induce a two-stage activation of the c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) in A431 cells; the early-stage JNK activation is singlet oxygen-dependent, whereas the late-stage JNK activation is mediated by the singlet oxygen-triggered caspase activation. Experiments using anti-sense oligonucleotides against JNK1 and PAK2 further show that during PDT-induced apoptosis the early-stage JNK activation is required for caspase activation, and that the late-stage JNK activation is regulated by the caspase-mediated cleavage/activation of PAK2. Collectively, a model for the PDT-triggered apoptotic signalling cascade with RB is proposed, which involves singlet oxygen, JNK, caspase-3 and PAK2, sequentially.

Effects of taspine on proliferation and apoptosis by regulating caspase-3 expression and the ratio of Bax/Bcl-2 in A431 cells

2010 ◽  
pp. n/a-n/a ◽  
Author(s):  
Yanmin Zhang ◽  
Qiao Jiang ◽  
Nan Wang ◽  
Bingling Dai ◽  
Yinnan Chen ◽  
...  
Keyword(s):  
Caspase 3 ◽  
A431 Cells ◽  
Proliferation And Apoptosis

Purging effect of dibutyl phthalate on leukemia cells involves fas independent activation of caspase-3/CPP32 protease

2002 ◽  
Vol 186 (2) ◽  
pp. 177-182 ◽  
Author(s):  
Li-Sheng Wang ◽  
Hong-Jun Liu ◽  
Jin-Hui Zhang ◽  
Chu-Tse Wu
Keyword(s):  
Caspase 3 ◽  
Dibutyl Phthalate ◽  
Leukemia Cells

scholarly journals The Anticancer Activity of Lycium barbarum Polysaccharide by Inhibiting Autophagy in Human Skin Squamous Cell Carcinoma Cells In Vitro and In Vivo

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Meihua Zeng ◽  
Qingtao Kong ◽  
Fang Liu ◽  
Jun Chen ◽  
Hong Sang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Survival Rate ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Nude Mice ◽  
Caspase 3 ◽  
A431 Cells ◽  
Lycium Barbarum

Objective. This study is aimed at investigating the effects of Lycium barbarum polysaccharide (LBP) on the proliferation and apoptosis of human cutaneous squamous cell carcinoma A431 cells in vitro and in vivo via its regulation on autophagy. Methods. In vitro experiment: A431 cells were treated with different concentrations of LBP, and cell viability was measured by the CCK8 method. Flow cytometry was used to detect the cell apoptosis rate. The expression of Ki67, PCNA, cl-caspase-3, Bcl-2, and LC3II and the phosphorylation status of JNK and ERK1/2, as well as the effect of SP600125 cotreatment on the expression of autophagy and apoptosis-associated proteins, were determined via Western blot. In vivo experiment: a transplanted tumor model was established by subcutaneous injection of A431 cells to the nude mice. 50 mg/kg LBP was injected into the mice intraperitoneally; the survival rate of mice, volume, and weight of tumor were determined on the 30th day. The expression of Ki67 and MMP-2 proteins was measured by immunohistochemistry. Results. LBP at concentrations of 400 μg/ml and above was significantly cytotoxic to A431 cells, whereas, within the dose range of 50 μg/ml~200 μg/ml, LBP significantly inhibited the expression of Ki67 and PCNA proteins, promoted the expression of cl-caspase-3, inhibited the expression of Bcl-2 protein, downregulated the expression of autophagy marker LC3II, and reduced the phosphorylation of ERK1/2, whereas the level of JNK phosphorylation was upregulated. At the same time, the regulation of Beclin1, LC3II, Bcl-2, and cl-caspase-3 by LBP was effectively reversed by the cotreatment of SP600125. In addition, LBP increased the survival rate of transplanted nude mice, reduced tumor volume and weight, and downregulated the expression of Ki67 and MMP-2. Conclusion. LBP can induce apoptosis of A431 cells by inhibiting autophagy and can inhibit tumor growth in vivo.

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