scholarly journals β-Sitosterol Induces Anti-proliferation and Apoptosis in Human Leukemic U937 Cells through Activation of Caspase-3 and Induction of Bax/Bcl-2 Ratio

2007 ◽  
Vol 30 (7) ◽  
pp. 1317-1323 ◽  
Author(s):  
Cheol Park ◽  
Dong-Oh Moon ◽  
Chung-Ho Rhu ◽  
Byung Tae Choi ◽  
Won Ho Lee ◽  
...  
Keyword(s):  
Caspase 3 ◽  
U937 Cells ◽  
Proliferation And Apoptosis

scholarly journals Effects of Silver Nanoparticles on Proliferation and Apoptosis in Granulosa Cells of Chicken Preovulatory Follicles: An In Vitro Study

Animals ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 1652
Author(s):  
Dorota Katarzyńska-Banasik ◽  
Anna Kozubek ◽  
Małgorzata Grzesiak ◽  
Andrzej Sechman
Keyword(s):  
Silver Nanoparticles ◽  
Granulosa Cells ◽  
Caspase 3 ◽  
In Vitro Study ◽  
Poultry Production ◽  
Cell Death Pathways ◽  
Preovulatory Follicles ◽  
Proliferation And Apoptosis ◽  
Apoptosis Process

The continuous development of poultry production related to the growing demand for eggs and chicken meat makes it necessary to use modern technologies. An answer to this demand may be the use of nanotechnology in poultry farming. One of the promising nanomaterials in this field are silver nanoparticles (AgNPs), which are used as disinfectants, reducing microbial pollution and the amounts of greenhouse gases released. This study aimed to evaluate the effect of AgNPs on the proliferation and apoptosis process in the granulosa cells of chicken preovulatory follicles. The in vitro culture experiment revealed that both 13 nm and 50 nm AgNPs inhibited the proliferation of the granulosa cells. However, a faster action was observed in 50 nm AgNPs than in 13 nm ones. A size-dependent effect of AgNP was also demonstrated for the caspase-3 activity. AgNPs 13 nm in size increased the caspase-3 activity in granulosa cells, while 50 nm AgNPs did not exert an effect, which may indicate the induction of distinct cell death pathways by AgNPs. In conclusion, our study reveals that AgNPs in vitro inhibit granulosa cell proliferation and stimulate their apoptosis. These results suggest that AgNPs may disrupt the final stage of preovulatory follicle maturation and ovulation.

Immunosuppressant PG490 (triptolide) induces apoptosis through the activation of caspase-3 and down-regulation of XIAP in U937 cells

2003 ◽  
Vol 66 (2) ◽  
pp. 273-280 ◽  
Author(s):  
Yun-Jung Choi ◽  
Tae Gyu Kim ◽  
Young-Ho Kim ◽  
Sung-Hee Lee ◽  
Young Kyu Kwon ◽  
...  
Keyword(s):  
Caspase 3 ◽  
U937 Cells ◽  
Down Regulation

scholarly journals Garcinol Alone and in Combination With Cisplatin Affect Cellular Behavior and PI3K/AKT Protein Phosphorylation in Human Ovarian Cancer Cells

Dose-Response ◽  
2020 ◽  
Vol 18 (2) ◽  
pp. 155932582092673
Author(s):  
Jie Zhang ◽  
Huan Fang ◽  
Jinguo Zhang ◽  
Wencai Guan ◽  
Guoxiong Xu
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Caspase 3 ◽  
Anticancer Agent ◽  
Nuclear Factor Κb ◽  
Ovarian Cancer Cells ◽  
Cellular Behavior ◽  
Proliferation And Apoptosis ◽  
Induced Apoptosis ◽  
Physiological Benefits

Garcinol is a plant-derived compound that has some physiological benefits to human cells. However, the effect of garcinol on ovarian cancer (OC) cell proliferation and apoptosis is unknown. The current study aimed to examine the effects of garcinol alone and in combination with cisplatin (DDP) on cellular behavior and to explore the expression pattern of PI3K/AKT and nuclear factor-κB (NF-κB) in human OC cells. We found that OVCAR-3 cell viability was decreased after garcinol treatment. Garcinol alone and in combination with DDP significantly inhibited cell proliferation and had a synergistic effect evaluated by CompuSyn software. The cell cycle analysis showed the S phase arrest by garcinol. Furthermore, garcinol alone and in combination with DDP promoted cell apoptosis. The garcinol-induced apoptosis was further confirmed by the detection of cleavage forms of PARP and caspase 3. An increase in proapoptotic factor Bax expression was also found in garcinol-treated cells. Moreover, garcinol significantly decreased the phosphorylation of PI3K and AKT proteins and downregulated the expression of NF-κB. Thus, our data demonstrated that garcinol has the potential to be used as an anticancer agent and may synergize the effect of DDP. These actions are most likely through the regulation of the PI3K/AKT and NF-κB pathways.

Human Monocytoid Leukemia Cells Are Highly Sensitive to Apoptosis Induced by 2′-Deoxycoformycin and 2′-Deoxyadenosine: Association With dATP-Dependent Activation of Caspase-3

Blood ◽  
1998 ◽  
Vol 92 (9) ◽  
pp. 3368-3375 ◽  
Author(s):  
Nozomi Niitsu ◽  
Yuri Yamaguchi ◽  
Masanori Umeda ◽  
Yoshio Honma
Keyword(s):  
Cell Lines ◽  
Caspase 3 ◽  
Lymphoma Cell ◽  
Leukemia Cells ◽  
Acute Monocytic Leukemia ◽  
U937 Cells ◽  
Monocytic Leukemia ◽  
Low Concentrations ◽  
American Society ◽  
Induced Apoptosis

Abstract The adenosine deaminase (ADA) inhibitor 2′-deoxycoformycin (dCF) significantly inhibits the proliferation of leukemia and lymphoma cell lines. When cells were incubated in the presence of both dCF and 2′-deoxyadenosine (dAd), the concentration of dCF required to induce apoptosis of monocytoid leukemia cells was much lower than that required for myeloid, erythroid, or lymphoma cell lines. Among the cell lines tested, U937 cells were the most sensitive to this treatment. The concentration of dCF that effectively inhibited the proliferation of U937 cells was 1/1,000 of that required for lymphoma cell lines, on a molar basis. However, the uptake of dCF or dAd in U937 cells was comparable with that in other leukemia and lymphoma cell lines. The intracellular accumulation of dATP in U937 cells was only slightly higher than that in other leukemia cells in dCF-treated culture. Treatment with dCF plus dAd induced apoptosis in U937 cells at low concentrations, and this apoptosis was reduced by treatment with caspase inhibitors. Induction of caspase-3 (CPP32) activity accompanied the apoptosis induced by dCF plus dAd. No activation of CPP32 was observed in cytosol prepared from exponentially growing leukemia and lymphoma cells. However, dATP effectively induced CPP32 activation in cytosol from monocytoid cells, but not in that from nonmonocytoid cells, suggesting that dATP-dependent CPP32 activation is at least partly involved in the preferential induction of apoptosis in monocytoid leukemia cells. The combination of dCF and dAd may be useful for the clinical treatment of acute monocytic leukemia. © 1998 by The American Society of Hematology.

scholarly journals HuR Affects Proliferation and Apoptosis of Chronic Lymphocytic Leukemia Cells via NF-κB Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Kai Xiao ◽  
Lin Yang ◽  
Xinfeng Gao ◽  
Ying An ◽  
Wei Xie ◽  
...  
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
B Lymphocytes ◽  
Caspase 3 ◽  
Human Tumor ◽  
Lymphocytic Leukemia ◽  
Cell Counting ◽  
Cell Sensitivity ◽  
Proliferation And Apoptosis ◽  
Potential Strategy ◽  
The Relationship

Objective. To investigate the effects of HuR protein on the treatment of chronic lymphocytic leukemia (CLL). Methods. LCL lymphoblast cells and B lymphocytes were subjected to HuR overexpression (OV) or interference (IV). Western blot was used to observe the protein expression of human tumor necrosis factor-associated factor 1 (TRAF1), human inhibitor of nuclear factor kappa-B kinase α (IKK-α), NF-κB-inducing kinase (NIK), and p52. Flow cytometry was performed to evaluate apoptosis, and the mRNA expression of TRAF1 was examined by quantitative reverse transcription polymerase chain reaction. Immunofluorescence was carried out to visualize the expression of HuR, and the relationship between HuR and TRAF1 was observed by pull-down test. Cell sensitivity to chlorambucil (CLB) and fludarabine (Flu) was assessed by Cell Counting Kit-8. Results. The expression of HuR and TRAF1 in LCLs was significantly increased compared to that in B lymphocytes. Compared with the control, HuR OV significantly increased the expression of TRAF1 (P<0.05), whereas it was significantly decreased in the IV group (P<0.05). HuR can bind to TRAF1 directly, and the binding rate is positively correlated with HuR expression. After inhibiting HuR, the expression of TRAF1, IKK-α, NIK, p52, pro-Caspase 3, and PARP was significantly upregulated in LCLs and B lymphocytes (P<0.05), while Caspase 3 was downregulated (P<0.05). Compared with the control, the proliferation of LCLs and B lymphocytes treated by CLB and Flu decreased significantly after HuR blockade (P<0.05). Conclusion. HuR may be a key protein regulating CLL resistance. After inhibiting HuR, inflammatory response and apoptosis were significantly increased, and the cell sensitivity to CLB and Flu increased, suggesting that inhibiting HuR activity may be a potential strategy to solve the problem of drug resistance in CLL cells.

Establishment of Persistent Infection with HIV-1 Abrogates the Caspase-3-Dependent Apoptotic Signaling Pathway in U937 Cells

1999 ◽  
Vol 247 (2) ◽  
pp. 514-524 ◽  
Author(s):  
Yasuharu Tanaka ◽  
Masanori Kameoka ◽  
Katsuya Ota ◽  
Asako Itaya ◽  
Kazuyoshi Ikuta ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Persistent Infection ◽  
Caspase 3 ◽  
U937 Cells ◽  
Apoptotic Signaling ◽  
Hiv 1

Clinical Significance of Circulating Ki-67 Protein and Caspase-3 Activity Levels in Patients with Acute Myeloid Leukemia.

Blood ◽  
2009 ◽  
Vol 114 (22) ◽  
pp. 3104-3104
Author(s):  
Jean-Marie Bruey ◽  
Hagop M. Kantarjian ◽  
Zeev Estrov ◽  
Wanlong Ma ◽  
Chen-Hsiung Yeh ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Caspase 3 ◽  
Lymphoblastic Leukemia ◽  
Activity Levels ◽  
Ki 67 ◽  
Control Subjects ◽  
Proliferation And Apoptosis ◽  
Acute Myeloid

Abstract Abstract 3104 Poster Board III-41 Ki-67 and caspase-3 are widely accepted as proliferation and apoptosis markers in human tumors. We recently reported that Ki-67 can be detected as a circulating protein (cKi-67) in the plasma of patients with acute lymphoblastic leukemia (ALL), and that higher levels in plasma correlated with more aggressive disease. Here we investigated the levels of cKI-67 in patients with acute myeloid leukemia (AML). Since both apoptosis and proliferation are interconnected in defining the biology of a cancer, we also evaluated the level of apoptosis in AML as determined by caspase-3 activity in plasma. The study included a group of 106 newly diagnosed AML patients and 98 normal control subjects. We used the Meso Scale Discovery system for determining the levels of cKi-67. Apoptosis was determined by measuring caspase-3 activity (DEVD) in the plasma using a standard enzymatic fluorogenic assay. Median (range) levels of cKi-67 were significantly higher in patients with AML than in control subjects (1301 [0-6789] ng/mL vs 339 [35.76-2830.65] ng/mL; P<0.0001), as were caspase-3 activity levels (11.9 [5.8-218.2] pmol/min vs 8.27 [4.54-34.30] pmol/min; P<0.0001). Neither cKi-67 level nor caspase-3 activity correlated with white cell count, hemoglobin, platelet count, lactate dehydrogenase, blast count, age, cytogenetic grouping, or performance status. However, high levels (above the upper quartile of 2100 ng/mL) of cKi-67 were significantly associated with longer survival among patients >70 years of age (n=84; P=0.02) and those with unfavorable cytogenetics (n=38; P=0.006). On the other hand, high levels of caspase-3 activity (above upper quartile of 14 pmol/min) were associated with shorter survival (P=0.02) irrespective of age or cytogenetic grouping. In conclusion, proliferation and apoptosis as determined by plasma cKi-67 level and caspase-3 activity are unusual in AML. In that, higher proliferation and lower apoptosis are associated with better survival, most likely reflecting that cells progressing through the cell cycle may respond better to chemotherapy. These measurements should be considered in new therapeutic approaches that target cell cycle. Disclosures No relevant conflicts of interest to declare.

scholarly journals Effects of bFGF on the Modulation of Apoptosis in Gingival Fibroblasts with Different Host Ages

2013 ◽  
Vol 2013 ◽  
pp. 1-7
Author(s):  
Kotaro Tanimoto ◽  
Satoru Ohkuma ◽  
Yuki Tanne ◽  
Ryo Kunimatsu ◽  
Naoto Hirose ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Proliferation ◽  
Caspase 3 ◽  
Type I Collagen ◽  
Pcr Analysis ◽  
Type I ◽  
Gingival Fibroblasts ◽  
Cultured Fibroblasts ◽  
Proliferation And Apoptosis ◽  
Young Subjects

The purpose of this study was to investigate the effects of basic fibroblast growth factor (bFGF) treatment on the proliferation and apoptosis of cultured gingival fibroblasts (GFs). Human GFs were isolated from the palatal gingival tissues of 16 healthy volunteers ranging in the age from 9 to 35 years old. Cultured GFs were subjected to the analyses for cell proliferation by ELISA assay, gene expression by RT-PCR analysis, and apoptosis potency by caspase-3 assay. The cell proliferation activity and gene expression of type-I collagen and caspase-3 activity were enhanced significantly by the treatment with bFGF in cultured GFs. Furthermore, the activity of caspase-3 in cultured GFs from young subjects was significantly higher than that in GFs from adults. It is shown that bFGF significantly enhances the gene expression of type-I collagen in cultured fibroblasts from human gingival tissues. It also demonstrated that bFGF modulates the apoptosis of periodontal fibroblasts, and the effect is higher in young subjects, indicating a significant role of bFGF in the prevention of scar formation during wound healing.

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