Cell viability and electrical response of breast cancer cell treated in aqueous graphene oxide solution deposition on interdigitated electrode

AbstractBreast cancer is one of the most reported cancers that can lead to death. Despite the advances in diagnosis and treatment procedures, the possibility of cancer recurrences is still high in many cases. With that in consideration, researchers from all over the world are showing interest in the unique features of Graphene oxide (GO), such as its excellent and versatile physicochemical properties, to explore further its potential and benefits towards breast cancer cell treatment. In this study, the cell viability and electrical response of GO, in terms of resistivity and impedance towards the breast cancer cells (MCF7) and normal breast cells (MCF10a), were investigated by varying the pH and concentration of GO. Firstly, the numbers of MCF7 and MCF10a were measured after being treated with GO for 24 and 48 h. Next, the electrical responses of these cells were evaluated by using interdigitated gold electrodes (IDEs) that are connected to an LCR meter. Based on the results obtained, as the pH of GO increased from pH 5 to pH 7, the number of viable MCF7 cells decreased while the number of viable MCF10a slightly increased after the incubation period of 48 h. Similarly, the MCF7 also experienced higher cytotoxicity effects when treated with GO concentrations of more than 25 µg/mL. The findings from the electrical characterization of the cells observed that the number of viable cells has corresponded to the impedance of the cells. The electrical impedance of MCF7 decreased as the number of highly insulating viable cell membranes decreased. But in contrast, the electrical impedance of MCF10a increased as the number of highly insulating viable cell membranes increased. Hence, it can be deduced that the GO with higher pH and concentration influence the MCF7 cancer cell line and MCF10a normal breast cell.

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Cell Viability And Electrical Response of Breast Cancer Cell Treated In Aquoes Graphene Oxide Solution Deposition On Interdigitated Electrode

10.21203/rs.3.rs-772026/v1 ◽

2021 ◽

Author(s):

Muhammad M. Ramli ◽

Anis Rosman ◽

Nur Mazlan ◽

Mohd Ahmad ◽

Dewi Che Halin ◽

...

Keyword(s):

Breast Cancer ◽

Graphene Oxide ◽

Cell Viability ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Electrical Impedance ◽

Electrical Response ◽

Normal Breast ◽

Mcf7 Cells ◽

Viable Cells

Abstract Breast cancer is one of the most reported cancers that can lead to death. Despite the advances in diagnosis and treatment procedures, the possibility of cancer recurrences is still high in many cases. With that in consideration, researchers from all over the world are showing interest in the unique features of Graphene oxide (GO), such as its excellent and versatile physicochemical properties, to explore further its potential and benefits towards breast cancer cell treatment. In this study, the cell viability and electrical response of GO, in terms of resistivity and impedance towards the breast cancer cells (MCF7) and normal breast cells (MCF10a), were investigated by varying the pH and concentration of GO. Firstly, the numbers of MCF7 and MCF10a were measured after being treated with GO for 24 and 48 hours. Next, the electrical responses of these cells were evaluated by using interdigitated electrodes (IDEs) gold electrodes that are connected to an E4980 20 Hz – 2 MHz Precision LCR meter. Based on the results obtained, as the pH of GO increased from pH 5 to pH 7, the number of viable MCF7 cells decreased while the number of viable MCF10a slightly increased after the incubation period of 48 hours. Similarly, the MCF7 also experienced higher cytotoxicity effects when treated with a GO concentration of more than 25 μg/mL. The findings from the electrical characterization of the cells observed that the number of viable cells has corresponded to the impedance of the cells. The electrical impedance of MCF7 decreased as the number of highly insulating viable cells membrane decreased, but in contrast, the electrical impedance of MCF10a increased as the number of highly insulating viable cells membrane increased. Hence, it can be deduced that the GO with higher pH and concentration impacts the MCF7 cancer cell line and MCF10a normal breast cell.

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Potential Metabolite Nymphayol Isolated from Water Lily (Nymphaea stellata) Flower Inhibits MCF-7 Human Breast Cancer Cell Growth via Upregulation of Cdkn2a, pRb2, p53 and Downregulation of PCNA mRNA Expressions

Metabolites ◽

10.3390/metabo10070280 ◽

2020 ◽

Vol 10 (7) ◽

pp. 280

Author(s):

Laila Naif Al-Harbi ◽

Pandurangan Subash-Babu ◽

Manal Abdulaziz Binobead ◽

Maha Hussain Alhussain ◽

Sahar Abdulaziz AlSedairy ◽

...

Keyword(s):

Breast Cancer ◽

Tumor Suppressor ◽

Cell Viability ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Kinase Inhibitor ◽

B Cell Lymphoma ◽

Nuclear Antigen ◽

Mrna Levels ◽

Mcf 7

Controlled production of cyclin dependent kinases (CDK) and stabilization of tumor suppressor genes are the most important factors involved in preventing carcinogenesis. The present study aimed to explore the cyclin dependent apoptotic effect of nymphayol on breast cancer MCF-7 cells. In our previous study, we isolated the crystal from a chloroform extract of Nymphaea stellata flower petals and it was confirmed as nymphayol (17-(hexan-2-yl)-10,13-dimethylhexadecahydro-1H-cyclopenta[a]phenanthren-3-ol) using x-ray diffraction (XRD), Fourier transform infrared (FTIR), and mass spectroscopy (MS) methods. The cytotoxic effect of nymphayol on MCF-7 cells were analyzed using the 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The cellular and nuclear damage was determined using propidium iodide (PI) and acridine orange/ethidium bromide (AO/ErBr) staining. Tumor suppressor and apoptosis related mRNA transcript levels were determined using real-time polymerase chain reaction (RT-PCR). Nymphayol potentially inhibits MCF-7 cell viability up to 78%, and the IC50 value was observed as 2.8 µM in 24 h and 1.4 µM in 48 h. Treatment with nymphayol significantly increased reactive oxygen species (ROS) level and the tunnel assay confirmed DNA damage. We found characteristically 76% apoptotic cells and 9% necrotic cells in PI and AO/ErBr staining after 48 h treatment with 2.8 µM of nymphayol. Gene expression analysis confirmed significantly (p ≤ 0.001) increased mRNA levels of cyclin dependent kinase inhibitor 2A (Cdkn2a), retinoblastoma protein 2 (pRb2), p53, nuclear factor erythroid 2-factor 2 (Nrf2), caspase-3, and decreased B-cell lymphoma 2 (Bcl-2), murine double minute 2 (mdm2), and proliferating cell nuclear antigen (PCNA) expression after 48 h. Nymphayol effectively inhibited breast cancer cell viability, and is associated with early expression of Cdkn2a, pRb2, and activation of p53 and caspases.

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ANTICANCER ACTIVITY OF SILVER NANOPARTICLES AGAINST HUMAN BREAST CANCER CELL LINE

Kongunadu Research Journal ◽

10.26524/krj282 ◽

2019 ◽

Vol 6 (1) ◽

pp. 25-29

Author(s):

Dinesh B ◽

Ranjithkumar R ◽

Sharmila C ◽

Selvam K ◽

Chandar Shekar B

Keyword(s):

Breast Cancer ◽

Cell Viability ◽

Cell Line ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cell Line ◽

Cancer Cell Line ◽

Green Technology ◽

Future Application ◽

Dose Dependent

The present study demonstrated the effectiveness of bioinspired synthesized AgNPs against MCF-7 breast cancer cell line, we found a dramatic decrease in cell viability when the concentration of the bioinspired synthesized AgNPs was increased and there was a dose-dependent reduction in cell viability. This study further indicates the significance of green technology for nanoparticle fabrication and future application in control of several human diseases.

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HOXD3 Plays a Critical Role in Breast Cancer Stemness and Drug Resistance

Cellular Physiology and Biochemistry ◽

10.1159/000489249 ◽

2018 ◽

Vol 46 (4) ◽

pp. 1737-1747 ◽

Cited By ~ 3

Author(s):

Yue Zhang ◽

Qingyuan Zhang ◽

Zhongru Cao ◽

Yuanxi Huang ◽

Shaoqiang Cheng ◽

...

Keyword(s):

Breast Cancer ◽

Drug Resistance ◽

Western Blot ◽

Cell Viability ◽

Cancer Cells ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Cancer Cells ◽

Rt Pcr ◽

Integrin Β3

Background/Aims: Homeobox D3 (HOXD3) is a member of the homeobox family of genes that is known primarily for its transcriptional regulation of morphogenesis in all multicellular organisms. In this study, we sought to explore the role that HOXD3 plays in the stem-like capacity, or stemness, and drug resistance of breast cancer cells. Methods: Expression of HOXD3 in clinical breast samples were examined by RT-PCR and immunohistochemistry. HOXD3 expression in breast cancer cell lines were analyzed by RT-PCR and western blot. Ability of drug resistance in breast cancer cells were elevated by MTT cell viability and colony formation assays. We examined stemness using cell fluorescent staining, RT-PCR and western blot for stem cell marker expression. Finally, activity of wnt signaling was analyzed by FOPflash luciferase assays. RT-PCR and western blot were performed for downstream genes of wnt signaling. Results: We demonstrated that HOXD3 is overexpressed in breast cancer tissue as compared to normal breast tissue. HOXD3 overexpression enhances breast cancer cell drug resistance. Furthermore, HOXD3 upregulation in the same cell lines increased sphere formation as well as the expression levels of stem cell biomarkers, suggesting that HOXD3 does indeed increase breast cancer cell stemness. Because we had previously shown that HOXD3 expression is closely associated with integrin β3 expression in breast cancer patients, we hypothesized that HOXD3 may regulate breast cancer cell stemness and drug resistance through integrin β 3. Cell viability assays showed that integrin β 3 knockdown increased cell viability and that HOXD3 could not restore cancer cell stemness or drug resistance. Given integrin β 3’s relationship with Wnt/β-catenin signaling, we determine whether HOXD3 regulates integrin β 3 activity through Wnt/β-catenin signaling. We found that, even though HOXD3 increased the expression of Wnt/β-catenin downstream genes, it did not restore Wnt/β-catenin signaling activity, which was inhibited in integrin β3 knockdown breast cancer cells. Conclusion: We demonstrate that HOXD3 plays a critical role in breast cancer stemness and drug resistance via integrin β3-mediated Wnt/β-catenin signaling. Our findings open the possibility for improving the current standard of care for breast cancer patients by designing targeted molecular therapies that overcome the barriers of cancer cell stemness and drug resistance.

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Quantification of prolactin receptor mRNA in multiple human tissues and cancer cell lines by real time RT-PCR

Journal of Endocrinology ◽

10.1677/joe.0.171r001 ◽

2001 ◽

Vol 171 (1) ◽

pp. R1-R4 ◽

Cited By ~ 62

Author(s):

SK Peirce ◽

WY Chen ◽

WY Chen

Keyword(s):

Breast Cancer ◽

Prostate Cancer ◽

Cell Lines ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Cancer Cell Lines ◽

Normal Breast ◽

Breast Cancer Cell Lines ◽

Human Tissues ◽

Normal Human

Human prolactin (hPRL) has been reported to be involved in breast and prostate cancer development. The hPRL receptor (hPRLR) is expressed in a wide variety of tissues in at least three isoforms. In this study, a one-step real time reverse transcription PCR technique was used to determine relative expression levels of hPRLR mRNA in eleven human breast cancer cell lines, HeLa cells, three prostate cancer cell lines and nine normal human tissues. The housekeeping gene beta-actin was used for internal normalization. We demonstrate that hPRLR mRNA is up-regulated in six of the eleven breast cancer cell lines tested when compared with normal breast tissue. Of the cancer cell lines tested, we found that T-47D cells have the highest level of hPRLR mRNA, followed by MDA-MB-134, BT-483, BT-474, MCF-7 and MDA-MB-453 cells. In two breast cancer cell lines (MDA-MB-468 and BT-549), the hPRLR levels were found to be comparable to that of normal breast tissue. Three breast cancer cell lines (MDA-MB-436, MDA-MB-157 and MDA-MB-231) expressed hPRLR mRNA at levels lower than that of normal tissue. In contrast, in all three commonly used prostate cancer cell lines (LNCaP, PC-3 and DU 145), the levels of hPRLR mRNA were found to be down-regulated relative to that of normal prostate tissue. Of nine normal human tissues tested, we found that the uterus and the breast have the highest levels of hPRLR mRNA, followed by the kidney, the liver, the prostate and the ovary. The levels of hPRLR mRNA were the lowest among the trachea, the brain and the lung.

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MicroRNA-203 Regulates Growth and Metastasis of Breast Cancer

Cellular Physiology and Biochemistry ◽

10.1159/000430331 ◽

2015 ◽

Vol 37 (1) ◽

pp. 35-42 ◽

Cited By ~ 22

Author(s):

Shan Zhao ◽

Jinzhu Han ◽

Likang Zheng ◽

Zixin Yang ◽

Li Zhao ◽

...

Keyword(s):

Breast Cancer ◽

Cell Cycle ◽

Cell Growth ◽

Cancer Cell ◽

Breast Cancer Cell ◽

Breast Tissue ◽

Normal Breast Tissue ◽

Normal Breast ◽

Cancer Cell Growth ◽

Breast Cancer Cell Growth

Backgrounds/Aims: MicroRNAs (MiRNAs) control many biological events and play critical roles in the development of tumor. Among all miRNAs, miR203 has been recently shown to have an inhibitory effect on prostate cancer. However, its involvement in the carcinogenesis of breast cancer has not been reported. Methods: We examined the levels of miR203 in the breast cancer from the patients compared to the paired normal breast tissue. We also examined the levels of miR203 in several commonly used breast cancer cell lines. The effects of overexpression or depletion of miR203 on breast cancer cell growth were analyzed by a MTT assay, and on breast cancer cell invasion were examined by a scratch wound healing assay and a transwell cell migration assay. MiR203-targeted genes were analyzed by Western blot. Results: We detected significantly lower levels of miR203 in the breast cancer from the patients compared to the paired normal breast tissue. Moreover, the levels of miR203 were significantly lower in breast cancer tissue from the patients with cancer metastasis. Decreased miR203 levels were detected in all examined breast cancer lines. Overexpression of miR203 inhibited breast cancer cell growth and invasion, while antisense-mediated inhibition of miR203 enhanced cancer cell growth and invasion. Further analyses show that miR203 may inhibit cell growth through decreasing cell-cycle activator cyclinD2 and CDK6, increasing cell-cycle suppressor p21 and p27, and increasing apoptosis-associated protein Bcl-2. MiR203 may also inhibit cell metastasis through suppressing matrix metalloproteinase 2 (MMP2), MMP7 and MMP9. Conclusion: Our data thus highlight miR203 as a novel therapeutic target for breast cancer.

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