scholarly journals Anticancer Activity of Leaf Hydro Ethanolic Extract of Aegle marmelos in Human Lung Cancer Cell Mediated through Caspase-3 and Caspase-9 mRNA Expression

2021 ◽  
pp. 336-343
Author(s):  
R. Sukanth ◽  
G. Sridevi ◽  
J. Selvaraj ◽  
S. Preetha
Keyword(s):  
Lung Cancer ◽  
Mrna Expression ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Leaf Extract ◽  
Caspase 3 ◽  
Fold Change ◽  
Lung Cancer Cells ◽  
Aegle Marmelos ◽  
Caspase 9

Background: Aegle marmelos (AE) is a medicinal plant that comes under the rutaceae family and the plant was used in the past for treating many diseases and illness symptoms. The plant has many effects such as anti-diarrhoeal, antimicrobial, antiviral, radioprotective, anticancer, chemopreventive, antipyretic, ulcer healing, antigenotoxic, diuretic, antifertility and anti-inflammatory properties. Aim: To know the anticancer activity of hydroethanolic leaf extract of Aegle marmelos over lung cancer cells treated with caspase 3 and caspase 9 mRNA expression. Materials and Methods: The required chemicals were collected mainly from Canada. The lung cancer cells (A549) were collected from NCCS pune and then RNA was extracted from the cells and then the study was conducted after treating it with caspase 3 and caspase 9 mRNA expression. The cells were treated with many dosage of hydroethanolic extract of Aegle marmelos and the cell viability was noted. Results: The study reported that extract of Aegle marmelos has a great anticancer activity about 1 fold change over rate of 1.7 for cells treated with caspase 3 and a fold change over of 1 in caspase 9 treated lung cancer cells. Conclusion: The study concluded an innovative finding that the hydroethanolic leaf extract of Aegle marmelos has a great anticancer activity against lung cancer cells treated with caspase 3 and caspase 9 mRNA expression.

scholarly journals Decoction of Chinese Herbal Medicine Fuzheng Kang-Ai Induces Lung Cancer Cell Apoptosis via STAT3/Bcl-2/Caspase-3 Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Sumei Wang ◽  
Shunqin Long ◽  
Shujing Xiao ◽  
Wanyin Wu ◽  
Swei Sunny Hann
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Lung Cancer Cells ◽  
Lung Cancer Cell ◽  
Caspase 9 ◽  
Chinese Herbal ◽  
Protein Expressions

Decoction of Chinese herbal medicine (CHM) Fuzheng Kang-Ai (FZKA for short) has been applied as adjuvant treatment strategy in advanced lung cancer patients for decades. We previously showed that FZKA decoction inhibited proliferation of non-small cell lung cancer (NSCLC) cells through activation of AMP-activated protein kinase alpha (AMPKα) signaling pathway, followed by inducing insulin-like growth factor (IGF) binding protein 1 (IGFBP1) and forkhead homeobox type O3a (FOXO3a) proteins, and enhanced the inhibition effect of gefitinib in lung cancer cell growth via inactivating PI3-K/Akt-mediated suppressing of cell surface-associated mucin-1 (MUC1) expression. In this study, we investigated the molecular mechanism by which FZKA decoction affected cell apoptosis in lung cancer cells. Our results show that FZKA induced apoptosis in lung cancer cells. Mechanistically, FZKA activated the caspase-3, PARP, and caspase-9 activities. Both antiapoptotic and proapoptotic proteins from Bcl-2 family were deregulated by FZKA exposure in lung cancer cells. In addition, FZKA reduced protein expressions of signal transducer and activator of transcription 3 (STAT3) and Jun activation domain-binding protein 1 (Jab1), while it concomitantly increased p21 protein. Moreover, the inhibitor of caspase-3 resisted the effect of FZKA on induction of apoptosis. Finally, exogenous overexpression of STAT3 overcame FZKA-inhibited protein expressions of Bcl-2 and myeloid cell leukemia-1 (Mcl-1) as well as Bax and blocked FZKA-induced activities of caspase-3 and caspase-9. Our results show that FZKA decoction promotes lung cancer cell apoptosis through STAT3/Bcl-2/caspase-3 signaling pathways. This study unveils potential novel molecular mechanism by which FZKA controls growth of human lung cancer cells.

Anticancer Activity of Platinum (II) Complex with 2-Benzoylpyridine by Induction of DNA Damage, S-Phase Arrest, and Apoptosis

2020 ◽  
Vol 20 (4) ◽  
pp. 504-517
Author(s):  
Yu-Lan Li ◽  
Xin-Li Gan ◽  
Rong-Ping Zhu ◽  
Xuehong Wang ◽  
Duan-Fang Liao ◽  
...  
Keyword(s):  
Dna Damage ◽  
B Cell ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Hepg2 Cells ◽  
Caspase 3 ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
S Phase ◽  
Caspase 9

Objective: To overcome the disadvantages of cisplatin, numerous platinum (Pt) complexes have been prepared. However, the anticancer activity and mechanism of Pt(II) complexed with 2-benzoylpyridine [Pt(II)- Bpy]: [PtCl2(DMSO)L] (DMSO = dimethyl sulfoxide, L = 2-benzoylpyridine) in cancer cells remain unknown. Methods: Pt(II)-Bpy was synthesized and characterized by spectrum analysis. Its anticancer activity and underlying mechanisms were demonstrated at the cellular, molecular, and in vivo levels. Results: Pt(II)-Bpy inhibited tumor cell growth, especially HepG2 human liver cancer cells, with a halfmaximal inhibitory concentration of 9.8±0.5μM, but with low toxicity in HL-7702 normal liver cells. Pt(II)- Bpy induced DNA damage, which was demonstrated through a marked increase in the expression of cleavedpoly (ADP ribose) polymerase (PARP) and gamma-H2A histone family member X and a decrease in PARP expression. The interaction of Pt(II)-Bpy with DNA at the molecular level was most likely through an intercalation mechanism, which might be evidence of DNA damage. Pt(II)-Bpy initiated cell cycle arrest at the S phase in HepG2 cells. It also caused severe loss of the mitochondrial membrane potential; a decrease in the expression of caspase-9 and caspase-3; an increase in reactive oxygen species levels; the release of cytochrome c and apoptotic protease activation factor; and the activation of caspase-9 and caspase-3 in HepG2 cells, which in turn resulted in apoptosis. Meanwhile, changes in p53 and related proteins were observed including the upregulation of p53, the phosphorylation of p53, p21, B-cell lymphoma-2-associated X protein, and NOXA; and the downregulation of B-cell lymphoma 2. Moreover, Pt(II)-Bpy displayed marked inhibitory effects on tumor growth in the HepG2 nude mouse model. Conclusion: Pt(II)-Bpy is a potential candidate for cancer chemotherapy.

Moringa oleifera: Natural leaf extract with potential anti-cancerous effect on A549 lung cancer cells

Lung Cancer ◽  
2012 ◽  
Vol 77 ◽  
pp. S22 ◽  
Author(s):  
M. Dany ◽  
N. Madi ◽  
N. Nemer ◽  
M. Beyrouthy ◽  
S. Abdoun ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Leaf Extract ◽  
Moringa Oleifera ◽  
Lung Cancer Cells ◽  
Natural Leaf ◽  
A549 Lung

Effect of Curcumin Coated with Polymethyl Methacrylate Nanoparticles on Lung Cancer Cells

2020 ◽  
Vol 12 (8) ◽  
pp. 1015-1021
Author(s):  
Ximiao Ma ◽  
Fangyong Fu
Keyword(s):  
Lung Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Polymethyl Methacrylate ◽  
Drug Loading ◽  
Lung Cancer Cells ◽  
Caspase 9 ◽  
Incidence And Mortality ◽  
High Incidence ◽  
Related Proteins

Lung cancer is a malignant tumor with an extremely high incidence and mortality rate in clinical practice and its pathogenesis remains unclear at present. Currently, the methods for treating this disease have relatively high limitations. However, with the gradual maturity and application of nanotechnology, a number of studies have pointed out that polymethyl methacrylate nanoparticles (PMMA-NPs) encapsulated with curcumin (Cur) possibly becomes a new and effective scheme for treating lung cancer. First of all, Cur-PMMA-NPs were prepared. Their sizes were determined by characterization techniques, and their effects on lung cancer cells A549 were detected by Cell proliferation experiment and flow cytometry. The expression of apoptosis-related proteins in the cells was detected by Western blotting. The results showed that polyacrylic acid (PAA)-Cur-PMMA-NPs had a particle size of (215.00±6.00) nm. The drug loading rate and the encapsulation rate of nanospheres were remarkably higher than those of free Cur (P < 0.05). After the intervention of PAA-Cur-PMMA-NPs in the cells, the cell proliferation and the Bcl-2 expression reduced, while the apoptotic rate and the expression of Bax, Caspase-3, and Caspase-9 increased (P < 0.05). Accordingly, Cur-PMMA-NPs can inhibit lung cancer cells from growth and induce their apoptosis, so they are expected to become an effective intervention measure to improve the therapeutic effect on lung cancer in the future.

Parathyroid hormone-related protein ameliorates death receptor-mediated apoptosis in lung cancer cells

2003 ◽  
Vol 285 (6) ◽  
pp. C1429-C1436 ◽  
Author(s):  
Randolph H. Hastings ◽  
Flavio Araiza ◽  
Douglas W. Burton ◽  
Lu Zhang ◽  
Maxwell Bedley ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Parathyroid Hormone ◽  
Cancer Cells ◽  
Uv Irradiation ◽  
Cancer Progression ◽  
Caspase 3 ◽  
Death Receptor ◽  
Related Protein ◽  
Caspase 9 ◽  
Parathyroid Hormone Related Protein

Parathyroid hormone-related protein (PTHrP) is expressed in more advanced, aggressive tumors and may play an active role in cancer progression. This study investigated the effects of PTHrP on apoptosis after UV irradiation, Fas ligation, or staurosporine treatment in BEN human squamous lung carcinoma cells. Cells at 70% confluency were treated for 24 h with 100 nM PTHrP-(1-34), PTHrP-(38-64), PTHrP-(67-86), PTHrP-(107-139), or PTHrP-(140-173) in media with serum, exposed for 30 min to UV-B radiation (0.9 mJ/cm2), and maintained for another 24 h. Caspase-3, caspase-8, and caspase-9 activities increased fivefold. Pretreatment with PTHrP-(1-34) and PTHrP-(140-173) ameliorated apoptosis after UV irradiation, as indicated by reduced caspase activities, increased cell protein, decreased nuclear condensation, and increased clonal survival. Other peptides had no effect on measures of apoptosis. PTHrP-(140-173) also reduced caspase activities after Fas ligation by activating antibody, but neither peptide had effects on caspase-3 or caspase-9 activity after 1 μM staurosporine. These data indicate that PTHrP-(1-34) and PTHrP-(140-173) protect against death receptor-induced apoptosis in BEN lung cancer cells but are ineffective against mitochondrial pathways. PTHrP contributes to lung cancer cell survival in culture and could promote cancer progression in vivo. The mechanism for the protective effect against apoptosis remains to be determined.

scholarly journals Combined anticancer activity of osthole and cisplatin in NCI-H460 lung cancer cells in vitro

2013 ◽  
Vol 5 (3) ◽  
pp. 707-710 ◽  
Author(s):  
XIAO-MAN XU ◽  
YI ZHANG ◽  
DAN QU ◽  
HONG-BO LIU ◽  
XIU GU ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Lung Cancer Cells

scholarly journals P3.01-064 The Overexpression and Cleavage of SASH1 by Caspase-3 Stimulates Cell Death in Lung Cancer Cells

2017 ◽  
Vol 12 (1) ◽  
pp. S1158-S1159
Author(s):  
Joshua Burgess ◽  
Emma Bolderson ◽  
Steven Gray ◽  
Martin Barr ◽  
Kathy Gately ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Caspase 3 ◽  
Lung Cancer Cells
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