scholarly journals (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) induces apoptosis via the intrinsic pathway in H1299 lung cancer cells

2017 ◽  
Author(s):  
Jong-Woon Shin ◽  
Sae-Bom Kwon ◽  
Yesol Bak ◽  
Sangku Lee ◽  
Do-Young Yoon
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Morphological Changes ◽  
A549 Cells ◽  
Fluorescein Isothiocyanate ◽  
Receptor Expression ◽  
Dependent Manner ◽  
Intrinsic Pathway ◽  
Extrinsic Pathway ◽  
Dose Dependent

Abstract(E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) is known as a dual specific phosphatase 1/6 or MAPK inhibitor. However, its precise anti-lung cancer mechanism remains unknown. In this study, the effects of BCI on cell viability were investigated in the non-small cell lung cancer cell lines NCI-H1299, A549, and NCI-H460. We confirmed that BCI significantly inhibited the cell viability of NCI-H1299 compared to those of NCI-H460 and A549 cells. The anti-cancer effects of BCI were evaluated by MTS assay, annexin V-fluorescein isothiocyanate/propidium iodide staining, cell cycle analysis, reverse transcription-PCR, western blotting, and JC-1 staining in NCI-H1299 cells. BCI induced cellular morphological changes and inhibited viability of NCI-H1299 cells in a dose-dependent manner. BCI enhanced Bax expression and induced processing of caspase-9, caspase-3, and poly (ADP-ribose) polymerase as well as the release of cytochrome c from the mitochondria into the cytosol. BCI also down-regulated Bcl-2 expression but enhanced Bax expression in a dose-dependent manner in NCI-H1299 cells. In addition, BCI did not modulate death receptor expression or the extrinsic factor caspase-8 and Bid, a linker between the intrinsic and extrinsic apoptotic pathways in NCI-H1299 cells. On the basis of these results, we conclude that BCI induces apoptosis through a mediated intrinsic pathway, but not extrinsic pathway in NCI-H1299 cells. These results suggest that BCI can be used as a therapeutic agent in lung cancer.

scholarly journals Cytotoxic Effects of Flubendazole in Human Lung Cancer Cell Line A549

2020 ◽  
Vol 11 (4) ◽  
Author(s):  
Elham Hoveizi ◽  
Fatemeh Fakharzadeh Jahromi
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Human Lung ◽  
A549 Cells ◽  
Beclin 1 ◽  
Human Lung Cancer ◽  
Pcr Analysis ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Acridine Orange Staining

Background: The development of effective anticancer drugs is a significant health issue. Previous studies showed that members of the benzimidazole family have anticancer effects on several cancers Objectives: The present study investigated the cytotoxic effect of flubendazole on A549 human lung cancer cells. Methods: The A549 cells were treated with flubendazole at 1, 2, 5, and 10 µM concentrations for three days. Cell viability was measured by the MTT assay and Acridine orange staining. Also, the expressions of P62 and Beclin -1 were analyzed by qRT-PCR analysis. Results: Cell viability of A549 cells, in a concentration-dependent manner, showed significant differences between the treatment and control groups, and the IC50 value was determined to be 2 µM. Also, flubendazole reduced the expression of P62 and increased the expression of Beclin 1 in treated cells. Conclusions: Flubendazole induces cell death in A549 cells in a dose and time-dependent manner and can offer new factors in lung cancer therapeutic strategies.

Apoptosis induced by microwave radiation in pancreatic cancer JF305 cells

2014 ◽  
Vol 92 (4) ◽  
pp. 324-329 ◽  
Author(s):  
Wenhe Zhu ◽  
Wei Zhang ◽  
Huiyan Wang ◽  
Junjie Xu ◽  
Yan Li ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Morphological Changes ◽  
Annexin V ◽  
Fluorescein Isothiocyanate ◽  
Dependent Manner ◽  
Therapeutic Approaches ◽  
Caspase 9 ◽  
New Therapeutic Approaches ◽  
Related Proteins ◽  
Dose Dependent

New therapeutic approaches are needed to improve the survival rate from pancreatic cancer, one of the most lethal human malignancies. In this study, JF305 cells were treated with microwaves at doses of 2.5, 5.0, 10.0, 15.0, and 20.0 mW/cm2 for 20 min. The inhibition of JF305 cell proliferation was tested using the MTT assay. Apoptotic cells were detected with Hoechst 33258 staining and a Nucleo-Counter NC-3000. The expression of apoptosis-related proteins was examined with Western blot. The results showed that microwaves inhibited the growth of JF305 cells in a dose–dependent manner, and caused morphological changes in apoptotic body formation. The percentages of apoptosis detected using annexin V–fluorescein isothiocyanate (FITC) were 4.0%, 10.0%, 12.0%, and 30.0% with the dosage of microwave (0, 5.0, 10.0, and 20.0 mW/cm2), respectively. Treatment with microwaves increased the activity of caspase-9 and caspase-3, down-regulated the expression of Bcl-2, and up-regulated the expression of Bax and CytoC. In addition, the expression level of p65 was increased whereas the level of IκBα down-regulated. Those results suggest that microwaves inhibit cell growth and induce apoptosis in JF305 cells through an NF-κB-regulated mitochondria-mediated pathway.

scholarly journals Influenza A Virus and Influenza B Virus Can Induce Apoptosis via Intrinsic or Extrinsic Pathways and Also via NF-κB in a Time and Dose Dependent Manner

2016 ◽  
Vol 2016 ◽  
pp. 1-14 ◽  
Author(s):  
Ibrahim El-Sayed ◽  
Khalid Bassiouny ◽  
Aziz Nokaly ◽  
Ahmed S. Abdelghani ◽  
Wael Roshdy
Keyword(s):  
Influenza A ◽  
A549 Cells ◽  
Influenza Viruses ◽  
Influenza B Virus ◽  
Influenza B ◽  
Caspase 8 ◽  
Dependent Manner ◽  
Intrinsic Pathway ◽  
Caspase 9 ◽  
Dose Dependent

Influenza viruses are able to cause annual epidemics and pandemics due to their mutation rates and reassortment capabilities leading to antigenic shifts and drifts. To identify host response to influenza A and B viruses on A549 and MDCK II cells at low and high MOIs, expressions of MxA and caspases 3, 8, and 9 and BAD, TNFα, and IκBαgenes were measured in the cells supernatants. H1N1 and H3N2 prefer to initially enhance the intrinsic pathway, determined by higher caspase 9 activity in MDCK II cells compared to caspase 8 activity and vice versa in A549 cells at different MOIs, while INF B prefers extrinsic pathway in A549 cells according to significant low or undetectable caspase 9 activity and high activity of caspase 8 but also can induce intrinsic pathway in MDCK II cells as determined by significant low or undetectable activity of caspase 8 and high caspase 9 activity at different MOIs; the considerable MxA expression was found in influenza A and B viruses infected A549 and MDCK II cells at low MOIs. In conclusion, influenza A and B viruses induced extrinsic and intrinsic apoptosis in parallel, and the induction was associated with viral infection in a dose dependent manner.

scholarly journals Enhancement of Phthalocyanine Mediated Photodynamic Therapy by Catechin on Lung Cancer Cells

Molecules ◽  
2020 ◽  
Vol 25 (21) ◽  
pp. 4874
Author(s):  
Giftson J. Senapathy ◽  
Blassan P. George ◽  
Heidi Abrahamse
Keyword(s):  
Lung Cancer ◽  
Dna Damage ◽  
Photodynamic Therapy ◽  
Side Effects ◽  
Cell Viability ◽  
Morphological Changes ◽  
A549 Cells ◽  
Treatment Method ◽  
Zinc Phthalocyanine ◽  
Photodynamic Therapy Of Cancer

Worldwide, lung cancer remains one of the leading cancers with increasing mortality rates. Though chemotherapy for lung cancer is effective, it is always accompanied by unavoidable and grave side effects. Photodynamic therapy (PDT), using novel photosensitizers, is an advanced treatment method with relatively few side effects. Plant products are emerging as potent photosensitizers (PSs). The dose-dependent effect of Catechin (CA) (20–100 µM) on cellular morphological changes, cell viability, cytotoxicity, proliferation, DNA damage and apoptosis were studied on A549 adenocarcinoma alveolar basal epithelial cells. The effect of CA, along with Zinc phthalocyanine PS at 680 nm and 5 J/cm2 fluency was also studied. As the doses of CA increased, the results showed a pattern of increased cytotoxicity, accompanied by decreased cell viability and proliferation in A549 cells. Also, at 52 µM (IC50), CA in combination with PS significantly increased the cytotoxicity, DNA damage, and apoptosis, as compared to control and PS alone, treated cells in PDT experiments. These findings leave a possible thread that CA can be used in the application of phyto-photodynamic therapy of cancer in future.

scholarly journals Hop-derived Xanthohumol Induces HL-60 Leukemia Cells Death

2020 ◽  
pp. 61-72
Author(s):  
M. Pacurari ◽  
H. Brown ◽  
A. Rieland
Keyword(s):  
Cell Viability ◽  
Cell Cycle Progression ◽  
Caspase 3 ◽  
Morphological Changes ◽  
Chromatin Condensation ◽  
Dependent Manner ◽  
Cycle Progression ◽  
Humulus Lupulus L ◽  
Additional Chemotherapy ◽  
Dose Dependent

Background: Acute promyelocytic leukemia (APL) affects both kids and adults, however it is more prevalent in younger population. Although APL has a favorable prognostic, patients that relapse often do not respond positively to additional chemotherapy. Therefore, there is a need to further identify ways to overcome these challenges.  Hypothesis: In this study, we examined antileukemic effects of xanthohumol (XN), a prenylated flavonoid derived from hops (Humulus lupulus L), on human promyelocytic HL-60 cells.  Materials and Methods: HL-60 cells were exposed to different concentrations of XN (μM) for 24 h. Cell viability, cell morphology, chromatin condensation, cPARP-1 level, and caspase-3 activation, and the expression of p21WAF1/Cip1 were analyzed. Results: XN reduced HL-60 cell viability in a dose-dependent manner. XN induced a dose-dependent morphological changes including cell shrinkage and blebbing, and significantly increased the number of cells with condensed chromatin. XN significantly increased the level of cPARP-1, active caspase-3, and the expression of p21WAF/CIP mRNA. Conclusion: These data indicate that XN induces HL-60 cell death by regulating cell cycle progression and apoptosis. This study suggests that XN may have antileukemic preventive effects.

scholarly journals Crocus sativusL. (Saffron) Stigma Aqueous Extract Induces Apoptosis in Alveolar Human Lung Cancer Cells through Caspase-Dependent Pathways Activation

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Saeed Samarghandian ◽  
Abasalt Borji ◽  
Seyed Kazem Farahmand ◽  
Reza Afshari ◽  
Saeideh Davoodi
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Aqueous Extract ◽  
Morphological Changes ◽  
Flow Cytometric Analysis ◽  
A549 Cells ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Induced Apoptosis

Worldwide, lung cancer is the most common form of cancer. Saffron has been used in folk medicine for centuries. We investigated the potential of saffron to induce cytotoxic and apoptotic effects in lung cancer cells (A549). We also examined the caspase-dependent pathways activation of saffron-induced apoptosis against the A549 cells. A549 cells were incubated with different concentrations of saffron extract; then cell morphological changes, cell viability, and apoptosis were determined by the normal invertmicroscope, MTT assay, Annexin V and propidium iodide, and flow cytometric analysis, respectively. Activated caspases were detected by treatment of saffron in lung cancer cells using fluorescein-labeled inhibitors of polycaspases. The proliferation of the A549 cells were decreased after treatment with saffron in a dose- and time-dependent manner. The percentage of apoptotic cells increased with saffron concentrations. Saffron induced morphological changes, decreased percentage of viable cells, and induced apoptosis. Saffron could induce apoptosis in the A549 cells and activate caspase pathways. The levels of caspases involved in saffron-induced apoptosis in the A549 cells indicating caspase-dependent pathway were induced by saffron. The anticancer activity of the aqueous extract of saffron could be attributed partly to its inhibition of the cell proliferation and induction of apoptosis in cancer cells through caspase-dependent pathways activation.

scholarly journals Investigating Cytotoxic Effects and Molecular Mechanisms of Quinoa Seed Extract Against Human Lung Cancer Cell Lines

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Homa Mollaei ◽  
Farzaneh Karimi ◽  
Morteza Ghorbany ◽  
Mahboubeh Sadat Hosseinzadeh ◽  
Maryam Moudi ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Viability ◽  
Cancer Cell ◽  
A549 Cells ◽  
Seed Extract ◽  
Human Lung Cancer ◽  
Dependent Manner ◽  
Lung Cancer Cell ◽  
Expression Levels ◽  
Seed Extracts

Background: Lung cancer is one of the most common leading causes of mortality and morbidity worldwide. Despite recent advances in therapeutic approaches, common methods are not fully effective. Thus, researchers are looking for some novel complementary agents to improve the effectiveness of therapies. Emerging evidence has shown the antitumor activity of several natural components such as quinoa seed extracts in various types of cancer. Objectives: Hence, this study was conducted to evaluate the antiproliferation and anti-apoptotic activity of quinoa on the A549 lung cancer cell line. Methods: The cell viability of A549 cells treated with quinoa was detected using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The expression levels of BAX and BCL2 as apoptosis-related genes were assessed using real-time polymerase chain reaction (PCR). Finally, the statistical analysis was performed using GraphPad Prism version 7. Results: Our findings demonstrated that the cell viability decreased in a concentration and time-dependent manner. Also, treating A549 cells with doses of 1.60 and 1.92 mg/mL of quinoa seed extracts could increase BAX and decrease BCL2 expression levels (P < 0.05). However, the higher dose (1.92 mg/mL) was significantly effective. Conclusions: According to this study, quinoa seed extract could induce apoptosis in lung cancer cells (A549) throughout the increased ratio of BAX/BCL2. However, further investigations are required to confirm the results.

VDAC1 Mediated Anticancer Activity of Gallic Acid in Human Lung Adenocarcinoma A549 Cells

2018 ◽  
Vol 18 (2) ◽  
pp. 255-262 ◽  
Author(s):  
Aikebaier Maimaiti ◽  
Amier Aili ◽  
Hureshitanmu Kuerban ◽  
Xuejun Li
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Gallic Acid ◽  
Molecular Mechanisms ◽  
A549 Cells ◽  
Dependent Manner ◽  
Lung Carcinoma Cells ◽  
Induced Apoptosis ◽  
The Impact

Aims: Gallic acid (GA) is generally distributed in a variety of plants and foods, and possesses cell growth-inhibiting activities in cancer cell lines. In the present study, the impact of GA on cell viability, apoptosis induction and possible molecular mechanisms in cultured A549 lung carcinoma cells was investigated. Methods: In vitro experiments showed that treating A549 cells with various concentrations of GA inhibited cell viability and induced apoptosis in a dose-dependent manner. In order to understand the mechanism by which GA inhibits cell viability, comparative proteomic analysis was applied. The changed proteins were identified by Western blot and siRNA methods. Results: Two-dimensional electrophoresis revealed changes that occurred to the cells when treated with or without GA. Four up-regulated protein spots were clearly identified as malate dehydrogenase (MDH), voltagedependent, anion-selective channel protein 1(VDAC1), calreticulin (CRT) and brain acid soluble protein 1(BASP1). VDAC1 in A549 cells was reconfirmed by western blot. Transfection with VDAC1 siRNA significantly increased cell viability after the treatment of GA. Further investigation showed that GA down regulated PI3K/Akt signaling pathways. These data strongly suggest that up-regulation of VDAC1 by GA may play an important role in GA-induced, inhibitory effects on A549 cell viability.

scholarly journals Effects of ambient particulate matter on a reconstructed human corneal epithelium model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ryota Ko ◽  
Masahiko Hayashi ◽  
Miho Tanaka ◽  
Tomoaki Okuda ◽  
Chiharu Nishita-Hara ◽  
...  
Keyword(s):  
Particulate Matter ◽  
Cell Viability ◽  
Corneal Epithelium ◽  
Dependent Manner ◽  
Ambient Particulate Matter ◽  
Tissue Sections ◽  
Human Corneal Epithelium ◽  
Vitro Model ◽  
Dose Dependent

AbstractWe evaluated the effects of ambient particulate matter (PM) on the corneal epithelium using a reconstructed human corneal epithelium (HCE) model. We collected two PM size fractions [aerodynamic diameter smaller than 2.4 µm: PM0.3–2.4 and larger than 2.4 µm: PM>2.4] and exposed these tissues to PM concentrations of 1, 10, and 100 µg/mL for 24 h. After exposure, cell viability and interleukin (IL) IL-6 and IL-8 levels were determined, and haematoxylin and eosin and immunofluorescence staining of the zonula occludens-1 (ZO-1) were performed on tissue sections. In addition, the effects of a certified reference material of urban aerosols (UA; 100 µg/mL) were also examined as a reference. The viability of cells exposed to 100 μg/mL UA and PM>2.4 decreased to 76.2% ± 7.4 and 75.4% ± 16.1, respectively, whereas PM0.3–2.4 exposure had a limited effect on cell viability. These particles did not increase IL-6 and IL-8 levels significantly even though cell viability was decreased in 100 μg/mL UA and PM>2.4. ZO-1 expression was reduced in a dose-dependent manner in all groups. Reconstructed HCE could be used as an in vitro model to study the effects of environmental PM exposure on ocular surface cell viability and inflammation.

scholarly journals The Olive Leaves Extract Has Anti-Tumor Effects against Neuroblastoma through Inhibition of Cell Proliferation and Induction of Apoptosis

Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2178
Author(s):  
Fabio Morandi ◽  
Veronica Bensa ◽  
Enzo Calarco ◽  
Fabio Pastorino ◽  
Patrizia Perri ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Viability ◽  
Cell Cycle Progression ◽  
Treatment Strategies ◽  
Annexin V ◽  
Dependent Manner ◽  
Induction Of Apoptosis ◽  
Dose Dependent

Neuroblastoma (NB) is the most common extra-cranial solid tumor of pediatric age. The prognosis for high-risk NB patients remains poor, and new treatment strategies are desirable. The olive leaf extract (OLE) is constituted by phenolic compounds, whose health beneficial effects were reported. Here, the anti-tumor effects of OLE were investigated in vitro on a panel of NB cell lines in terms of (i) reduction of cell viability; (ii) inhibition of cell proliferation through cell cycle arrest; (iii) induction of apoptosis; and (iv) inhibition of cell migration. Furthermore, cytotoxicity experiments, by combining OLE with the chemotherapeutic topotecan, were also performed. OLE reduced the cell viability of NB cells in a time- and dose-dependent manner in 2D and 3D models. NB cells exposed to OLE underwent inhibition of cell proliferation, which was characterized by an arrest of the cell cycle progression in G0/G1 phase and by the accumulation of cells in the sub-G0 phase, which is peculiar of apoptotic death. This was confirmed by a dose-dependent increase of Annexin V+ cells (peculiar of apoptosis) and upregulation of caspases 3 and 7 protein levels. Moreover, OLE inhibited the migration of NB cells. Finally, the anti-tumor efficacy of the chemotherapeutic topotecan, in terms of cell viability reduction, was greatly enhanced by its combination with OLE. In conclusion, OLE has anti-tumor activity against NB by inhibiting cell proliferation and migration and by inducing apoptosis.

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