scholarly journals Effect of Hydroalcoholic Extract of Ephedramajor, Memordia charantia, and Resveratrol on Cytotoxicity and Caspase-3 Genes Expression Level in MCF-7 Breast Cancer Cell Line

2021 ◽  
Vol In Press (In Press) ◽  
Author(s):  
Seyed Kazem Sabbagh ◽  
Ehsan Ghodrati ◽  
Alireza Hajibeiki ◽  
Mahta Mazaheri ◽  
Mohammad Reza Sarafraz Ardakani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Medicinal Plants ◽  
Cell Viability ◽  
Cell Line ◽  
Plant Extracts ◽  
Caspase 3 ◽  
Cell Toxicity ◽  
Hydroalcoholic Extract ◽  
Expression Levels ◽  
Mcf 7

Background: To increase the therapeutic effect of drugs to combat diseases, combination therapy with current chemical drugs and new medicines derived from medicinal plants is necessary. Objectives: The present work aimed to investigate the effect of hydroalcoholic extract of two medicinal plants, Ephedra major and Momordi cacharantia (Carla), and resveratrol drug on cell viability and expression levels of caspase-3 gene in MCF-7 cell line. Methods: In this experimental study, the hydroalcoholic extraction of tested plants was done with a Soxhlet extractor. The MTT assay and real-time PCR were used to determine cell toxicity and caspase-3 gene expression levels, respectively. Results: The highest and lowest cytotoxic effects of plant extracts and resveratrol were observed at concentrations of 500 and 150 µg/mL, respectively. The highest level of the caspase-3 gene expression was observed after 72 h of incubation by different concentrations of plant extracts and resveratrol. Conclusions: It can be concluded that both plant extracts could influence cell viability in MCF-7 cells via the increase of cell toxicity and expression of caspase3 gene. Thus, these species could be used in the pharmaceutical industry.

scholarly journals Biological Effect of Organically Coated Grias neuberthii and Persea americana Silver Nanoparticles on HeLa and MCF-7 Cancer Cell Lines

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Lizeth Salazar ◽  
María José Vallejo López ◽  
Marcelo Grijalva ◽  
Luis Castillo ◽  
Alexander Maldonado
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Hela Cells ◽  
Biological Effect ◽  
Persea Americana ◽  
Expression Levels ◽  
Mcf 7

The aim of this study was to assess the biological effect of organically coated Grias neuberthii (piton) fruit and Persea americana (avocado) leaves nanoparticles (NPs) on cervical cancer (HeLa) and breast adenocarcinoma (MCF-7) cells with an emphasis on gene expression (p53 transcription factor and glutathione-S-transferase GST) and cell viability. UV-Vis spectroscopy analysis showed that synthesized AgNPs remained partially stable under cell culture conditions. HeLa cells remained viable when exposed to piton and avocado AgNPs. A statistically significant, dose-dependent cytotoxic response to both AgNPs was found on the breast cancer (MCF-7) cell line at concentrations above 50 µM. While expression levels of transcription factor p53 showed downregulation in treated MCF-7 and HeLa cells, GST expression was not affected in both cell lines treated. Cell viability assays along with gene expression levels in treated MCF-7 cells support a cancer cell population undergoing cell cycle arrest. The selective toxicity of biosynthesized piton/avocado AgNPs on MCF-7 cells might be of value for novel therapeutics.

scholarly journals The Synergistic Combination of Cisplatin and Piperine Induces Apoptosis in MCF-7 Cell Line

2021 ◽  
Author(s):  
Abolfazl Fattah ◽  
Ali Morovati ◽  
Zahra Niknam ◽  
Ladan Mashouri ◽  
Amirhooman Asadi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cell Line ◽  
Cancer Cell ◽  
Breast Cancer Cells ◽  
Caspase 3 ◽  
Assay Method ◽  
Caspase 9 ◽  
Mcf 7

Background: Piperine is a natural compound obtained from the Piper nigrum that exhibits anti-proliferative and anti-cancer activity in cancer cell lines. We analyzed the cytotoxic effect of piperine combined with cisplatin compound in the human MCF-7 breast cancer cell line and the underlying mechanism. Methods: The present in vitro study was performed on MCF-7 cell line in Jahrom University of Medical Sciences between, Jahrom, Iran from 2016 to 2017. Cultured MCF-7 cells were seeded into four groups: a control group (untreated group), a group treated with cisplatin, a group treated with piperine and a group treated with cisplatin and piperine. Cell viability was analyzed using the MTT assay method. Flow c-ytometric analysis was investigated for apoptosis. The mRNA and protein expression of the apoptotic regulators p53, Bcl-2, Bax, caspase 3 and caspase 9 were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting analysis. Results: Piperine (20 and 30 µM) in combination with cisplatin (5, 10 and 15 µM) for 24 h synergistically inhibited cell viability of MCF-7 breast cancer cells more than piperine and cisplatin used alone. Synergistic antibreast cancer activities cisplatin (5 µM) and piperine (20 µM) were via inducing apoptosis. Piperine (20 µM) and cisplatin (5 µM) for 24 h induce apoptosis strongly through reduction of Bcl-2 and increase of caspase 3, p53, caspase 9, and Bax. Conclusion: Piperine in combination with cisplatin could trigger p53-mediated apoptosis more effective than cisplatin alone in MCF-7 breast cancer cells, reducing the toxic dose of cisplatin used in cancer chemotherapy.

scholarly journals The Effect of Micro RNA-34a and carboplatin combination on the inducing apoptosis of Breast Cancer Cell line

2021 ◽  
Author(s):  
Sajjad Eslamkhah ◽  
Nazila Alizadeh ◽  
Sahar Safaei ◽  
Mohammad Amini ◽  
ahad Mokhtarzadeh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cell Line ◽  
Caspase 3 ◽  
Cancer Cell Line ◽  
Micro Rna ◽  
Control Group ◽  
Expression Levels ◽  
Micro Rnas

Abstract Aim: Breast cancer (BC) has been classified among the main causes of death owing to females' cancer. Carboplatin is a platinum-based chemotherapeutic drug that is an important treatment option for BC. But high and frequent doses of carboplatin usually reducing the reaction of cancer cells to medication. There is an immediate need to establish methods for increasing the carboplatin susceptibility to BC cells. For instance, micro RNAs (miRNAs) such as MiR34a demonstrate significant potential. Considering that, this research was planned to explore the better clinical effect and underlying mechanism of miR-34a as a possible tumor inhibitor and drug resistance regulator in compound with carboplatin chemotherapy drug in the cell lines of BC in humans. Methods: MCF-7 cell line was transfected with miR-34a to perform functional analyses. Subsequently, the MTT assay was applied to assess cell viability. Cell viability and cell death associated gene expression amounts including Bax, Bcl-2, caspase-3, MDR1, P53, and mir34-a, were examined through real-time quantitative PCR. Results: Findings showed that miR-34a upregulation significantly decreased MCF7 cell viability in comparison with control group. Furthermore, separate treatment of cells with miR-34a mimics and carboplatin could significantly increase Bax, Caspase-3, P53, and decrease in Bcl-2 mRNA expression levels evaluated to the non-treated group. Moreover, by reduction in expression levels of the MDR1 gene, BC cells' reaction to carboplatin has increased via miR-34a. Conclusion: In line with the findings, it could be inferred that miR-34a may improve the responsiveness of breast cancer cells to carboplatin chemotherapy with downregulation of MDR1.

Breviscapine Induces Breast Cancer Cell Cycle Arrest and Apoptosis by Modulating the Jak-Stat Pathway

2019 ◽  
Vol 18 (1) ◽  
pp. 83-88
Author(s):  
Zhang Lan ◽  
Lu Yuqin ◽  
Yin Siyuan ◽  
Luo Yaobing
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Viability ◽  
Cyclin D1 ◽  
Cell Cycle Arrest ◽  
Caspase 3 ◽  
Expression Levels ◽  
Cycle Arrest ◽  
Mcf 7 ◽  
Stat Pathway

The aim of this study was to investigate the effects and possible mechanisms of breviscapine arrest in the development of breast cancer cells. Cell viability, cycle arrest, and apoptosis were measured using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazoliumbromide assay and flow cytometry in MCF-7 cells treated with increasing concentrations of breviscapine. In addition, the expression level of cyclin D1, p21, cleaved caspase-3, and poly ADP-ribose polymerase, p-Janus kinase 2 and p-signal transducers and activators of transcription 3 was analyzed using western blot assay. The results showed that breviscapine suppressed cell viability and induced apoptosis in MCF-7 cells in a dose-dependent fashion. Breviscapine also increased MCF-7 cell number in the G1 phase and decreased that in the S phase. Moreover, cyclin D1, p-JAK2/JAK2, and p-STAT3/STAT3 expression levels were down-regulated, while p21, cleaved caspase-3, and poly ADP-ribose polymerase expression levels were up-regulated in breviscapine-treated MCF-7 cells. In conclusion, breviscapine regulates breast cancer viability, cell cycle arrest, and apoptosis in a concentration-dependent manner by modulating the JAK-STAT pathway.

Design, Synthesis and In Vitro Anti-Cancer Evaluation of Novel Derivatives of 2-(2-Methyl-1,5-diaryl-1H-pyrrol-3-yl)-2-oxo-N-(pyridin-3- yl)acetamide

2020 ◽  
Vol 16 (3) ◽  
pp. 340-349
Author(s):  
Ebrahim S. Moghadam ◽  
Farhad Saravani ◽  
Ernest Hamel ◽  
Zahra Shahsavari ◽  
Mohsen Alipour ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Peripheral Neuropathy ◽  
Cell Line ◽  
Normal Cell ◽  
Caspase 3 ◽  
Annexin V ◽  
Normal Cell Line ◽  
Anti Cancer ◽  
Mcf 7

Objective: Several anti-tubulin agents were introduced for the cancer treatment so far. Despite successes in the treatment of cancer, these agents cause toxic side effects, including peripheral neuropathy. Comparing anti-tubulin agents, indibulin seemed to cause minimal peripheral neuropathy, but its poor aqueous solubility and other potential clinical problems have led to its remaining in a preclinical stage. Methods: Herein, indibulin analogues were synthesized and evaluated for their in vitro anti-cancer activity using MTT assay (on the MCF-7, T47-D, MDA-MB231 and NIH-3T3 cell lines), annexin V/PI staining assay, cell cycle analysis, anti-tubulin assay and caspase 3/7 activation assay. Results: One of the compounds, 4a, showed good anti-proliferative activity against MCF-7 cells (IC50: 7.5 μM) and low toxicity on a normal cell line (IC50 > 100 μM). All of the tested compounds showed lower cytotoxicity on normal cell line in comparison to reference compound, indibulin. In the annexin V/PI staining assay, induction of apoptosis in the MCF-7 cell line was observed. Cell cycle analysis illustrated an increasing proportion of cells in the sub-G-1 phase, consistent with an increasing proportion of apoptotic cells. No increase in G2/M cells was observed, consistent with the absence of anti-tubulin activity. A caspase 3/7 assay protocol showed that apoptosis induction by more potent compounds was due to activation of caspase 3. Conclusion: Newly synthesized compounds exerted acceptable anticancer activity and further investigation of current scaffold would be beneficial.

SOX4 Serves an Oncogenic Role in the Tumourigenesis of Human Breast Adenocarcinoma by Promoting Cell Proliferation, Migration and Inhibiting Apoptosis

2020 ◽  
Vol 15 (1) ◽  
pp. 49-58
Author(s):  
Junhe Zhang ◽  
Shujie Chai ◽  
Xinyu Ruan
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Caspase 3 ◽  
Breast Adenocarcinoma ◽  
Migration Ability ◽  
Expression Levels ◽  
Apoptosis Rate ◽  
And Migration ◽  
Mcf 7 ◽  
Proliferation And Migration

Background: Breast cancer is among the most common malignant cancers worldwide, and breast adenocarcinoma in glandular tissue cells has excessive metastasis and invasion capability. However, little is known on the molecular process by which this disease develops and progresses. Objective: In this study, we explored the effects of sex-determining region Y-box 4 (SOX4) protein on proliferation, migration, apoptosis and tumourigenesis of breast adenocarcinoma and its possible mechanisms. Methods: The SOX4 overexpression or knockdown Michigan Cancer Foundation-7 (MCF-7) cell lines were established. Among the SOX4 overexpression or MCF-7 knockdown cell lines, proliferation, migration ability and apoptosis rate were detected. The expression levels of apoptosis-related proteins (Bax and Cleaved caspase-3) were analysed using Western blot. The effect of SOX4 on tumourigenesis was analysed using the clone formation assay in vitro and tumour xenograft experiment in nude mice. Results: Compared with the overexpression of control cells, proliferation and migration ability of SOX4 overexpression cells significantly increased, the apoptosis rate significantly decreased in addition to the expression levels of Bax and Cleaved caspase-3 (P < 0.05). Compared with the knockdown of control cells, proliferation and migration ability of SOX4 knockdown cells significantly decreased, and the apoptosis rate and expression levels of Bax and Cleaved caspase-3 significantly increased (P < 0.05). Clone formation and tumour growth abilities of SOX4 overexpression cells were significantly higher than those of the control cells (P < 0.05), whereas SOX4 knockdown cells had the opposite effect. Conclusion: SOX4 plays an oncogenic role in breast adenocarcinoma tumourigenesis by promoting cell proliferation, migration and inhibiting apoptosis. It can be used as a potential molecular target for breast cancer gene therapy.

Design, synthesis, molecular docking and ADME studies of novel indole-thiazolidinedione derivatives and their antineoplastic activity as CDK6 inhibitors

2021 ◽  
Author(s):  
Zeynep Ates-Alagoz ◽  
Mehmet Murat Kisla ◽  
Fikriye Zengin Karadayi ◽  
Sercan Baran ◽  
Tuğba Somay Doğan ◽  
...  
Keyword(s):  
Gene Expression ◽  
Molecular Docking ◽  
Anticancer Activity ◽  
Cell Line ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Antineoplastic Activity ◽  
Design Synthesis ◽  
Mcf 7

Several indole-thiazolidinedione derivatives (9–24) were designed and synthesized as CDK6 inhibitors, and their anticancer activity was probed on the MCF-7 cell line and the effects on gene expression profiles were elucidated.

scholarly journals Qingxin Kaiqiao Fang Inhibits Aβ25-35-Induced Apoptosis in Primary Cultured Rat Hippocampal Neuronal Cells via the p38 MAPK Pathway: An Experimental Validation and Network Pharmacology Study

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Tian-Qi Wang ◽  
Xiao-Xiao Lai ◽  
Lu-Ting Xu ◽  
Yan Shen ◽  
Jian-Wei Lin ◽  
...  
Keyword(s):  
Cell Viability ◽  
P38 Mapk ◽  
Caspase 3 ◽  
Mapk Pathway ◽  
Neuronal Cells ◽  
Neuronal Morphology ◽  
Cell Counting ◽  
Network Pharmacology ◽  
Expression Levels ◽  
P38 Mapk Pathway

Qingxin kaiqiao fang (QKF), a traditional Chinese medicine compound, has been applied to treat Alzheimer’s disease (AD) for many years and has exhibited remarkable effects. However, the underlying mechanism is still not explicit. The current study aims to investigate whether QKF exerts an antiapoptotic role through the p38 MAPK pathway in the course of AD. Network pharmacology analysis was applied to study the effective components, possible therapeutic targets, and AD-related pathway of QKF. Further, the AD cell model was established using amyloid-beta (Aβ)25-35 peptide and primary hippocampal neuronal cells extracted from newborn Sprague-Dawley rats. Microtubule-associated protein-2 (MAP-2) imaging was used to detect the morphology of hippocampal neurons. Western blot (WB) analysis was applied to detect the protein expression levels of p38 MAPK, p-p38 MAPK, Bcl-2, Bax, caspase-3, and cleaved caspase-3. Cell viability and apoptosis were determined using cell counting kit-8 (CCK-8) and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assays, respectively. SB203580 and U46619 were used to detect changes in cell morphology, cell viability, and apoptosis upon inhibiting or activating p38 MAPK. Our present work showed that QKF protects hippocampal neuronal morphology, enhances cell viability, and reduces the number of TUNEL-positive cells. In addition, our results showed that QKF increased the expression levels of antiapoptotic proteins and decreased the expression of proapoptotic proteins. QKF at 25 mg·mL−1 best inhibited neuronal apoptosis among the three doses of QKF by suppressing p38 MAPK activity. Collectively, QKF plays an antiapoptotic role via the p38 MAPK pathway.

scholarly journals Pituitary Adenylate Cyclase Activating Polypeptide Elicits Neuroprotection Against Acute Ischemic Neuronal Cell Death Associated with NMDA Receptors

2018 ◽  
Vol 51 (4) ◽  
pp. 1982-1995 ◽  
Author(s):  
Yuji Kaneko ◽  
Julian P. Tuazon ◽  
Xunming Ji ◽  
Cesario V. Borlongan
Keyword(s):  
Cell Death ◽  
Adenylate Cyclase ◽  
Protein Expression ◽  
Cell Viability ◽  
Caspase 3 ◽  
High Mobility ◽  
High Mobility Group ◽  
Expression Levels ◽  
Pituitary Adenylate Cyclase ◽  
Nmdar Subunits

Background/Aims: The endogenous neurotrophic peptides pituitary adenylate cyclase-activating polypeptides (PACAP-27/38) protect against stroke, but the molecular mechanism remains unknown. Methods: Primary rat neural cells were exposed to PACAP-27 or PACAP-38 before induction of experimental acute ischemic stroke via oxygen-glucose deprivation-reperfusion (OGD/R) injury. To reveal PACAP’s role in neuroprotection, we employed fluorescent live/dead cell viability and caspase 3 assays, optical densitometry of mitochondrial dehydrogenase and cell growth, glutathione disulfide luciferase activity, ELISA for high mobility group box1 extracellular concentration, ATP bioluminescence, Western blot analysis of PACAP, NMDA subunits, apoptosis regulator Bcl-2, social interaction hormone oxytocin, and trophic factor BDNF, and immunocytochemical analysis of PACAP. Results: Both PACAP-27 and PACAP-38 (PACAP-27/38) increased cell viability, decreased oxidative stress-induced cell damage, maintained mitochondrial activity, prevented the release of high mobility group box1, and reduced cytochrome c/caspase 3-induced apoptosis. PACAP-27/38 increased the protein expression levels of BDNF, Bcl-2, oxytocin, and precursor PACAP. N-methyl-D-aspartate receptor (NMDAR)-induced excitotoxicity contributes to the cell death associated with stroke. PACAP-27/38 modulated the protein expression levels of NMDAR subunits. PACAP-27/38 increased the protein expression levels of the GluN1 subunit, and decreased that of the GluN2B and GluN2D subunits. PACAP-27, but not PACAP-38, increased the expression level of the GluN2C subunit. Conclusion: This study provides evidence that PACAP regulated NMDAR subunits, affording neuroprotection after OGD/R injury.

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