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Artificial Cells, Nanomedicine, and... Dec 2023In order to load metformin in a nano formula and evaluate the produced nano form towards cancer cells, metformin was loaded on natural carrier coconut oil. The formed...
In order to load metformin in a nano formula and evaluate the produced nano form towards cancer cells, metformin was loaded on natural carrier coconut oil. The formed metformin-loaded coconut oil nanoemulsion was characterized by Zeta potential, particle size, drug content, drug release, and drug stability. The formed nanoemulsion was evaluated towards MCF-7, HepG2, and HCT-116 cell lines. Cell cycle analysis and apoptosis mechanism were studied. The nanoemulsion was created using deionized water, 1.5% Span 20, 1.5% Tween 80, 1.5% coconut oil, and 0.5% Metformin in an ultrasonicator to produce a homogenous solution. The anticancer activities of the metformin-loaded coconut nanoemulsion were highly improved compared to non-formulated metformin with IC50s of 8.3 ± 0.1 µg/ml, 12 ± 1.5 µg/ml, 2.685 ± 0.3 µg/ml for MCF-7, HepG2, and HCT-116 cell lines, respectively. There was a 76.5 ± 2.3 and 78.3 ± 3.2% increase in the number of apoptotic cells of MCF-7 and HepG2 cells after nanoemulsion treatment. This formula may be considered a new anticancer medication.
Topics: Humans; Coconut Oil; HCT116 Cells; MCF-7 Cells; Apoptosis; Cocos; Metformin
PubMed: 37589599
DOI: 10.1080/21691401.2023.2246145 -
Molecules (Basel, Switzerland) Feb 2022Three-dimensional cell culture has become a reliable method for reproducing in vitro cellular growth in more realistic physiological conditions. The surface...
Three-dimensional cell culture has become a reliable method for reproducing in vitro cellular growth in more realistic physiological conditions. The surface hydrophobicity strongly influences the promotion of cell aggregate formation. In particular, for spheroid formation, highly water-repellent coatings seem to be required for the significant effects of the process. In this work, surfaces at different wettability have been compared to observe their influence on the growth and promotion of aggregates of representative mammalian cell lines, both tumoral and non-tumoral (3T3, HaCat and MCF-7 cell lines). The effect of increased hydrophobicity from TCPS to agarose hydrogel to mixed organic-inorganic superhydrophobic (SH) coating has been investigated by optical and fluorescence microscopy, and by 3D confocal profilometry, in a time scale of 24 h. The results show the role of less wettable substrates in inducing the formation of spheroid-like cell aggregates at a higher degree of sphericity for the studied cell lines.
Topics: 3T3 Cells; Animals; Cell Culture Techniques; Cell Proliferation; Humans; Hydrogels; Hydrophobic and Hydrophilic Interactions; MCF-7 Cells; Mice; Spheroids, Cellular
PubMed: 35209035
DOI: 10.3390/molecules27041247 -
Analytical Chemistry Jun 2023Label-free electrochemical visualization of cancer cell apoptosis is essential for cancer therapies. In this work, we proposed a noninvasive imaging method using a...
Label-free electrochemical visualization of cancer cell apoptosis is essential for cancer therapies. In this work, we proposed a noninvasive imaging method using a light-addressable electrochemical sensor (LAES) for label-free imaging of drug-induced tumor cell apoptosis. The dynamic AC photocurrent changes on MCF-7 human breast adenocarcinoma cells after inducing by tamoxifen were imaged. And the reasons for photocurrent changes on the cells were explored by monitoring the changes in the ζ potentials of cells and Faradic impedance. The results demonstrated that the AC photocurrent on apoptotic MCF-7 cells increased, and the apoptosis degree of each cell was heterogeneous. Moreover, the AC photocurrent increase was attributed to the increased cell membrane permeability and the increased gap between the cell basal surface and the substrate caused by cell apoptosis. This study provides a brand new approach for label-free visualizing cell apoptosis heterogeneity, which has great potential in apoptosis-associated drug screening or drug efficacy evaluation.
Topics: Humans; Female; Apoptosis; Tamoxifen; Breast Neoplasms; MCF-7 Cells
PubMed: 37249570
DOI: 10.1021/acs.analchem.3c00566 -
Journal of Applied Biomaterials &... 2022Analyze the antitumor capacity of cetylpyridinium chloride (CPC) on human breast tumor cells, and the possible action mechanism.
OBJECTIVE
Analyze the antitumor capacity of cetylpyridinium chloride (CPC) on human breast tumor cells, and the possible action mechanism.
MATERIAL AND METHODS
The human breast tumor cells MCF-7 and no-tumor breast cells MCF-10A were exposed to CPC under various condition (concentration and duration). Cell viability was measured with MTT assay, the LIVE/DEAD assay, and fluorescence microscopy. Membrane permeability after CPC exposure was evaluated by Calcein AM assay, mitochondrial morphology with a MitoView staining, and genotoxicity with the comet assay and fluorescence microscopy.
RESULTS
CPC was cytotoxic to both MCF-7 and MCF-10A as of a 24-h exposure to 0.1 µM. Cytotoxicity was dose-dependent and reached 91% for MCF-7 and 78% for MCF-10A after a 24-h exposure to 100 µM CPC, which outperformed the positive control doxorubicin in effectiveness and selectivity. The LD50 of CPC on was 6 µM for MCF-7 and 8 µM for MCF-10A, yielding a selectivity index of 1.41. A time response analysis revealed 64% dead cells after only 5 min of exposure to 100 µM CPC. With respect to the action mechanisms, the comet assay did not reveal genome fragmentation. On the other hand, membrane damage was dose-dependent and may also affect mitochondrial morphology.
CONCLUSION
Cetylpyridinium chloride inhibits MCF-7 cell growing in a non-selective way as of 5 min of exposure. The action mechanism of CPC on tumor cells involves cell membrane damage without change neither mitochondrial morphology nor genotoxicity.
Topics: Antineoplastic Agents; Breast Neoplasms; Cell Survival; Cetylpyridinium; Female; Humans; MCF-7 Cells
PubMed: 35485910
DOI: 10.1177/22808000221092157 -
Journal of Natural Products May 20211-Deoxynojirimycin, an α-glucosidase inhibitor, possesses various biological activities such as antitumor, antidiabetic, and antiviral effects. However, the application...
1-Deoxynojirimycin, an α-glucosidase inhibitor, possesses various biological activities such as antitumor, antidiabetic, and antiviral effects. However, the application of 1-deoxynojirimycin is restricted by its poor lipophilicity and low bioavailability. In this study, three 1-deoxynojirimycin derivatives (-) comprising 1-deoxynojirimycin and kaempferol were designed and synthesized to modify their pharmacokinetics and improve their antitumor efficacy. Among them, compound , a conjugate of 1-deoxynojirimycin and kaempferol linked through an undecane chain, exhibited excellent lipophilicity, antiproliferative effects, and α-glucosidase inhibitory activity. Compared with 1-deoxynojirimycin, kaempferol, and their combination, compound downregulated cyclooxygenase-2 (COX-2) expression, arrested the cell cycle at the S phase, induced cellular apoptosis, and inhibited the migration of MCF-7 cells. Moreover, further investigation indicated that compound induced MCF-7 cell apoptosis through a mitochondrial-mediated pathway via the loss of mitochondrial membrane potential. This led to increasing intracellular levels of reactive oxygen species (ROS) and Ca, the downregulation of Bcl-2 expression, and the upregulation of Bax levels.
Topics: 1-Deoxynojirimycin; Apoptosis; Calcium; Cell Cycle Checkpoints; Humans; Kaempferols; MCF-7 Cells; Membrane Potential, Mitochondrial; Mitochondria; Proto-Oncogene Proteins c-bcl-2; Reactive Oxygen Species
PubMed: 33979163
DOI: 10.1021/acs.jnatprod.1c00014 -
Journal of Biochemical and Molecular... Oct 2022Developing new anticancer agents are crucial for cancer treatment. Antiproliferative activity of L1H as a bis-structured Schiff base was subjected to preliminary...
Developing new anticancer agents are crucial for cancer treatment. Antiproliferative activity of L1H as a bis-structured Schiff base was subjected to preliminary research in eight different kinds of cell lines by the cell viability method using different concentrations to determine their inhibitory concentration. L1H demonstrated the highest cytotoxicity in human breast cancer cell line MCF-7. In this perspective, the MCF-7 cell line was cultured for the examination of different molecular techniques, including MTT, apoptosis analysis by enzyme-linked immunosorbent assay (ELISA), and comet assay. Moreover, the DNA ladder, acridine orange/ethidium bromide as another apoptotic cell analysis, markers of oxidative stress, and total antioxidant status, total thiol, and GSH as nonenzymatic antioxidants assay were conducted. The above techniques have proven that L1H is a growth inhibitor effect when compared to cisplatin as a positive control in human breast cancer cells, especially those affected by L1H. The findings clearly show that L1H evaluated in MCF-7 cell lines causes rising or induced apoptosis, DNA damage, diminished antioxidant status against the increase of oxidized protein, and prevents cell proliferation. Manifold evidence supported our hypothesis that L1H has a potential therapeutically improved effect against the MCF-7 cell line, and then without a doubt is a suitable candidate drug for investigating cancers next.
Topics: Acridine Orange; Antineoplastic Agents; Antioxidants; Apoptosis; Breast Neoplasms; Cell Proliferation; Cisplatin; DNA; DNA Damage; Ethidium; Female; Growth Inhibitors; Humans; MCF-7 Cells; Schiff Bases; Sulfhydryl Compounds
PubMed: 35719061
DOI: 10.1002/jbt.23148 -
Journal of the American Chemical Society Jan 2020Effective and cell-type-specific delivery of CRISPR/Cas9 gene editing elements remains a challenging open problem. Here we report the development of biomimetic cancer...
Effective and cell-type-specific delivery of CRISPR/Cas9 gene editing elements remains a challenging open problem. Here we report the development of biomimetic cancer cell coated zeolitic imidazolate frameworks (ZIFs) for targeted and cell-specific delivery of this genome editing machinery. Coating ZIF-8 that is encapsulating CRISPR/Cas9 (CC-ZIF) with a cancer cell membrane resulted in the uniformly covered C-ZIF. Incubation of C-ZIF with MCF-7, HeLa, HDFn, and aTC cell lines showed the highest uptake by MCF-7 cells and negligible uptake by the healthy cells (i.e., HDFn and aTC). As to genome editing, a 3-fold repression in the EGFP expression was observed when MCF-7 were transfected with C-ZIF compared to 1-fold repression in the EGFP expression when MCF-7 were transfected with C-ZIF. In vivo testing confirmed the selectivity of C-ZIF to accumulate in MCF-7 tumor cells. This supports the ability of this biomimetic approach to match the needs of cell-specific targeting, which is unquestionably the most critical step in the future translation of genome editing technologies.
Topics: Animals; Biomimetics; CRISPR-Cas Systems; HeLa Cells; Heterografts; Humans; MCF-7 Cells; Metal-Organic Frameworks; Mice
PubMed: 31931564
DOI: 10.1021/jacs.9b11638 -
Anticancer Research Dec 2021Effect of capsicodendrin on the NF-κB pathway was studied in MCF-7 cancer cells.
BACKGROUND/AIM
Effect of capsicodendrin on the NF-κB pathway was studied in MCF-7 cancer cells.
MATERIALS AND METHODS
The transcription factor assay was used to screen for NF-κB activity. The effect on IKKβ, ICAM-1, and caspase-7 were studied using western blot. Caspase-1 was studied using Promega Caspase-Glo assay. Reactive oxygen species (ROS) were detected using the fluorescent probe DCFH-DA. The potentiometric dye JC-1 was used to assess mitochondrial membrane potential (ΔΨm) and the cell cycle was examined using a fluorescence-activated cell sorter.
RESULTS
NF-κB p65 inhibitory effect was IC=8.6 μM and cytotoxic activity was IC=7.5 μM. The upstream IKK and the downstream ICAM-1 were down-regulated. Sub G-phase population increased to 81% after 12 h of treatment with capsicodendrin (10 μM) and there was no loss of ΔΨM.
CONCLUSION
Increased levels of intracellular ROS promoted activity of caspase-1 and induced cell death in MCF-7 cells. Capsicodendrin may be a future anticancer agent that prevents the progression of metastatic breast cancer.
Topics: Antineoplastic Agents, Phytogenic; Caspases; Cell Cycle; Cinnamomum; Female; Humans; I-kappa B Kinase; MCF-7 Cells; Membrane Potential, Mitochondrial; Molecular Structure; NF-kappa B; Plant Extracts; Reactive Oxygen Species; Signal Transduction
PubMed: 34848447
DOI: 10.21873/anticanres.15412 -
Naunyn-Schmiedeberg's Archives of... Nov 2023The effects of insulin on the doxorubicin (Dox) sensitivity of breast cancer cell line MCF-7 and its Dox-resistant counterpart MCF-7/Dox were studied and glucose...
The effects of insulin on the doxorubicin (Dox) sensitivity of breast cancer cell line MCF-7 and its Dox-resistant counterpart MCF-7/Dox were studied and glucose metabolism, content of essential minerals, and the expression of several microRNAs in these cells upon exposure to insulin and Dox were compared. Cell viability colorimetric assay, colorimetric enzymatic technique, flow cytometry, immunocytochemical techniques, inductively-coupled plasma atomic emission spectroscopy, and quantitative polymerase chain reaction were used in the study. We found that insulin in high concentration significantly suppressed Dox toxicity, especially in parental MCF-7 cell line. The increase in proliferative activity triggered by insulin in MCF-7 but not MCF-7/Dox cells occurred in the setting of the increased level of specific binding sites for insulin and increased glucose uptake. Insulin treatment of MCF-7 cells in low and high concentrations resulted in the increase of Mg, Ca, and Zn content while in DOX-resistant cells, only Mg content increased upon exposure to insulin. High concentration of insulin increased the expression of kinase Akt1, P-glycoprotein 1 (P-gp1) and DNA excision repair protein ERCC-1 in MCF-7 cells, while in MCF-7/Dox cells, Akt1 expression decreased, and cytoplasmic expression of P-gp1 increased. In addition, insulin treatment affected expression of miR-122-5p, miR-133a-3p, miR-200b-3p, and miR-320a-3p. The decreased manifestation of biological effects of insulin in Dox-resistant cells could be partly explained by the different patterns of energy metabolism in MCF-7 cells and their Dox-resistant counterpart.
Topics: Female; Humans; Breast Neoplasms; Doxorubicin; Drug Resistance, Neoplasm; Insulin; MCF-7 Cells; MicroRNAs
PubMed: 37231169
DOI: 10.1007/s00210-023-02516-3 -
Mathematical Biosciences and... Jul 2019Breast cancer is the second most commonly diagnosed cancer in women worldwide. MCF-7 cell line is an extensively studied human breast cancer cell line. This cell line...
Breast cancer is the second most commonly diagnosed cancer in women worldwide. MCF-7 cell line is an extensively studied human breast cancer cell line. This cell line expresses estrogen receptors, and the growth of MCF-7 cells is hormone dependent. In this study, a mathematical model, which governs MCF-7 cell growth with interaction among tumor cells, estradiol, natural killer (NK) cells, cytotoxic T lymphocytes (CTLs) or CD8+ T cells, and white blood cells (WBCs), is proposed. Experimental data are used to determine functional forms and parameter values. Breast tumor growth is then studied using the mathematical model. The results obtained from numerical simulation are compared with those from clinical and experimental studies. The system has three coexisting stable equilibria representing the tumor free state, a microscopic tumor, and a large tumor. Numerical simulation shows that an immune system is able to eliminate or control a tumor with a restricted initial size. A healthy immune system is able to effectively eliminate a small tumor or produces long-term dormancy. An immune system with WBC count at the low parts of the normal ranges or with temporary low NK cell count is able to eliminate a smaller tumor. The cytotoxicity of CTLs plays an important role in immune surveillance. The association between the circulating estradiol level and cancer risk is not significant.
Topics: Breast Neoplasms; CD8-Positive T-Lymphocytes; Cell Line, Tumor; Cell Proliferation; Computer Simulation; Estradiol; Female; Humans; Immune System; Killer Cells, Natural; Leukocytes; MCF-7 Cells; Models, Theoretical; Receptor, ErbB-2; Receptors, Estrogen
PubMed: 31698574
DOI: 10.3934/mbe.2019325