scholarly journals Evaluation the effect of several anticancer drugs on Vietnamese breast cancer cells

2018 ◽  
Vol 21 (2) ◽  
pp. 44-51
Author(s):  
Oanh Thi-Kieu Nguyen
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Breast Cancer Cells ◽  
Multidrug Resistant ◽  
Positive Control ◽  
Breast Cancer Patients ◽  
Ic50 Value ◽  
Very High ◽  
Mcf 7

In Viet Nam, data from Conference of Cancer organized by the Ministry of Health has shown that breast cancer is the most popular cancer in women. Current mainly treatments are surgery, chemotherapy, and radiotherapy. However, the rate of recurrence after five years was very high. One of the causes of high relapse is cancer cells develop multidrug-resistant (MDR) thus reduced the efficiency of treatments. In this research, MTT assay was used for measured cell viability of Vietnamese breast cancer cells (VNBRCA cells) and positive control MCF-7 cell lines after treatment with several anticancer drugs as Doxorubicin (DOX), Tamoxifen (TAM), Mitomycin C (MMC) in 48h. After that, cancer cells were treated at haft maximal inhibitory concentration (IC50) of anticancer drug and observed cell morphology, apoptosis of cellular nuclear by AO/PI staining. IC50 value of VNBRCA cells with DOX, TAM, MMC were 0.641± 0.07 µM, 4.639 ± 0.933 µM and 1.338 ± 0.176 µM, respectively, which higher than IC50 of MCF-7 with DOX, TAM, MMC was 0.168 ± 0.037 µM, 7.085 ± 0.87 µM and 0.379 ± 0.159 µM, respectively. The response of VNBRCA cells with several anticancer drugs as DOX, TAM, and MMC was lower than the response of MCF-7, therefore, it showed that the specific features of VNBRCA cells; from which develop specific treatments for Vietnamese breast cancer patients.

scholarly journals ERβ-induced MFN2 inhibits the migration and invasiveness of breast cancer cells by inhibiting the P-AKT signaling pathway

2020 ◽  
Author(s):  
Mengyu Wei ◽  
Jun Hao ◽  
Xiaomei Liao ◽  
Yinfeng Liu ◽  
Ruihuan Fu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Akt Pathway ◽  
Cancer Cell Migration ◽  
Breast Cancer Patients ◽  
Human Breast ◽  
Mcf 7

Abstract Background Mitofusin 2 (MFN2) is localized on the outer membrane of mitochondria and is closely related to the migration of malignant tumor cells. Estrogen receptor β (ERβ) plays an anticancer role in breast cancer. Our previous experiments showed that ERβ can induce MFN2 expression, which then inhibits breast cancer cell migration. However, the exact mechanism by which ERβ-induced MFN2 inhibits breast cancer cell migration is unknown. Methods In this study, immunohistochemistry was first used to detect the expression of MFN2 in breast cancer tissues, and its relationship with the clinicopathological characteristics and prognosis of breast cancer patients was analyzed. MCF-7 and MDA-MB-231 cells were transfected with ERβ and MFN2 knockdown or expression plasmids. Western blot was used to detect the effects of ERβ on MFN2 and MFN2 on P-AKT473 and MMP2; the P-AKT pathway inhibitor LY294002 was administered to cells transfected with MFN2 knockdown plasmids, Western blot, immunocytofluorescence, and a wound healing assay revealed the effect of MFN2 on its downstream signaling pathway and the migration of breast cancer cells. Results This study found that the expression of MFN2 is related to the molecular type and prognosis of breast cancer patients ( P <0.05). The positive expression rate of MFN2 in triple-negative breast cancer was significantly lower than that in the HER2 + and luminal types. However, MFN2 expression was unrelated to age, tumor size, lymph node metastasis, TNM stage, histological type and grade ( P >0.05); ERβ positively regulated MFN2 expression and reduced the migration of both MCF-7 and MDA-MB-231 cells, while MFN2 knockdown increased the expression of P-AKT473 and MMP2. In contrast, the overexpression of MFN2 inhibited the expression of P-AKT473 and MMP2. These results showed that in MFN2 knockdown cells treated with LY294002, P-AKT473 and MMP2 expression levels were reversed. The reversal of P-AKT473 and MMP2 expression levels inhibits the invasiveness of human breast cancer cells. Conclusion MFN2 is related to the molecular subtype and prognosis of breast cancer. In human breast cancer MCF-7 and MDA-MB-231 cells, ERβ-induced MFN2 can inhibit the P-AKT pathway, which inhibits the invasiveness and migration of both breast cancer cell lines.

scholarly journals The Synthesis of Cinchonine Tiglat Ester Compound and Cytotoxic Test Against MCF-7 Breast Cancer Cell

2018 ◽  
Vol 19 (2) ◽  
pp. 54-61
Author(s):  
Ahmad Khanifudin ◽  
Gian Primahana ◽  
Sylvia Rizky Prima ◽  
Puspa Dewi Lotulung ◽  
Muhammad Hanafi
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cinchona Alkaloid ◽  
Alamar Blue ◽  
Tiglic Acid ◽  
Spectroscopy Instrumentation ◽  
Ic50 Value ◽  
Pass Through ◽  
Mcf 7

Cinchonine is a type of cinchona alkaloid compound commonly found and/or isolated from Cinchona sp. plant. It is commonly used to treat malaria, and can potentially be used against cancer cells. In this particular study, cinchonine ester derivatives were extracted through esterification processs. Synthesized esther is aimed to gain higher lipophilicity of cinchonine so that makes it easier to pass through cell membrane. Esterification was done using DCC activator as well as DMAP catalyst with tiglic acid used to create cinchonine tiglat. Subsequent cinchonine tiglat was obtained in the form of oil with 25,28% yield. The compound obtained from the synthesis was the analyzed using LC-ESI-MS and 1H-NMR spectroscopy instrumentation. Results show that the target compound has been successfully synthesized. Its cytotoxic ability against MCF-7 breast cancer cells was tested using the Alamar Blue method. Results concluded that cinchonine tiglat ester compound has a viable cytotoxic activity with IC50 value of 1.22 ppm.

scholarly journals Induction of multidrug resistance associated protein 2 in tamoxifen-resistant breast cancer cells

2007 ◽  
Vol 14 (2) ◽  
pp. 293-303 ◽  
Author(s):  
Hoo Kyun Choi ◽  
Jin Won Yang ◽  
Sang Hee Roh ◽  
Chang Yeob Han ◽  
Keon Wook Kang
Keyword(s):  
Breast Cancer ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Transcriptional Activation ◽  
Breast Cancer Cells ◽  
Pregnane X Receptor ◽  
Pi3 Kinase ◽  
Gene Promoters ◽  
Breast Cancer Patients ◽  
Mcf 7

Acquired resistance to tamoxifen (TAM) is a serious therapeutic problem in breast cancer patients. The transition from chemotherapy-responsive breast cancer cells to chemotherapy-resistant cancer cells is mainly accompanied by the increased expression of multidrug resistance-associated proteins (MRPs). In this study, it was found that TAM-resistant MCF-7 (TAMR-MCF-7) cells expressed higher levels of MRP2 than control MCF-7 cells. Molecular analyses using MRP2 gene promoters supported the involvement of the pregnane X receptor (PXR) in MRP2 overexpression in TAMR-MCF-7 cells. Although CCAAT/enhancer-binding protein β was overexpressed continuously in TAMR-MCF-7 cells, this might not be responsible for the transcriptional activation of the MRP2 gene. In addition, the basal activities of phosphatidylinositol 3-kinase (PI3-kinase) were higher in the TAMR-MCF-7 cells than in the control cells. The inhibition of PI3-kinase significantly reduced both the PXR activity and MRP2 expression in TAMR-MCF-7 cells. Overall, MRP2 induction plays a role in the additional acquisition of chemotherapy resistance in TAM-resistant breast cancer.

Synthesis, structures and biomolecular interactions of new silver(i) 5,5-diethylbarbiturate complexes of monophosphines targeting Gram-positive bacteria and breast cancer cells

2017 ◽  
Vol 46 (25) ◽  
pp. 8110-8124 ◽  
Author(s):  
Veysel T. Yilmaz ◽  
Ceyda Icsel ◽  
Jenaidullah Batur ◽  
Seyma Aydinlik ◽  
Murat Cengiz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Antimicrobial Activity ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Biomolecular Interactions ◽  
High Antimicrobial Activity ◽  
Gram Positive ◽  
Gram Positive Bacteria ◽  
Very High ◽  
Mcf 7

New silver(i) 5,5-diethylbarbiturate complexes exhibit very high antimicrobial activity against Gram-positive bacteria and kill MCF-7 cells, damaging mitochondria and DNA.

scholarly journals Suppression of αvβ6 downregulates P-glycoprotein and sensitizes multidrug-resistant breast cancer cells to anticancer drugs

Neoplasma ◽  
2020 ◽  
Vol 67 (02) ◽  
pp. 379-388 ◽  
Author(s):  
Y.H. ZHANG ◽  
Z.F. GAO ◽  
G.H. DONG ◽  
X. LI ◽  
Y. WU ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Anticancer Drugs ◽  
Breast Cancer Cells ◽  
Multidrug Resistant ◽  
P Glycoprotein

scholarly journals Downregulation of mdr-1 expression by 8-Cl-cAMP in multidrug resistant MCF-7 human breast cancer cells.

1995 ◽  
Vol 96 (2) ◽  
pp. 1026-1034 ◽  
Author(s):  
S Scala ◽  
A Budillon ◽  
Z Zhan ◽  
Y S Cho-Chung ◽  
J Jefferson ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Multidrug Resistant ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Mdr 1 ◽  
Mcf 7

scholarly journals CYTOTOXIC ACTIVITY AND SELECTIVITY INDEX OF BINAHONG (Anredera cordifolia) EXTRACTS ON MCF-7 BREAST CANCER CELLS AND VERO NORMAL CELLS LINE

2021 ◽  
Vol 3 (2) ◽  
pp. 72-80
Author(s):  
Dita Sozianty ◽  
Rifki Febriansah
Keyword(s):  
Breast Cancer ◽  
Cytotoxic Activity ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Selectivity Index ◽  
Cytotoxic Agents ◽  
Flavonoid Compounds ◽  
Ic50 Value ◽  
Her 2 ◽  
Mcf 7

Background: Breast cancers occur because of an impaired balance between proliferation, differentiation, and apoptosis of breast glands. Natural products have potency as cytotoxic agents with less side effects than chemotherapy. One of the potential plants is Anredera cordifolia (Ten.) Stennis (binahong), which contains flavonoid 8-glucopyranosyl- 4’,5,7-trihydroxy flavone compounds.Objective: This study aims to determine the potency of binahong leaves extract as an anticancer for breast cancer in vitro and in silico.Methods: Preliminary tests using molecular docking of 8-glucopyranosyl-4’,5,7-trihydroxyflavone compounds on Bcl-2 and HER-2 proteins. The extraction and fractionation were to obtain binahong extract. Thin layer chromatography to identify flavonoid compounds in the extract. DPPH assay was performed to evaluate the antioxidant activity. MTT assay was performed to evaluate cytotoxic activity on MCF-7 breast cancer cells and Vero cells.Results: In silico test showed a stable bond between 8-glucopyranosyl- 4’,5,7-trihydroxylflavone, and Bcl-2 and HER-2 with a docking score of -7.5 kcal/mol and -8.0 kcal/mol, respectively. The binahong extract contain flavonoid compounds that had the retention factor value 0.78; 0.49; 0.35. Antioxidant test resulted IC50 value of 4940 μg/mL. Cytotoxic test resulted in IC50 value of 1073 μg/mL and 486 μg/mL for Vero cells and MCF-7 breast cancer cells, respectively. The comparison between IC50 produced a selectivity index value of 2.149, which shows that binahong extract was selective against MCF-7 breast cancers.Conclusion: This study concluded that binahong extract has weak potency as anticancer agent on MCF-7 cells.

scholarly journals miR-200 affects tamoxifen resistance in breast cancer cells through regulation of MYB

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yu Gao ◽  
Wenzhi Zhang ◽  
Chengwen Liu ◽  
Guanghua Li
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tamoxifen Resistance ◽  
Breast Cancer Patients ◽  
Over Expression ◽  
Er Positive ◽  
Emt Markers ◽  
Mcf 7 ◽  
Positive Breast Cancer

AbstractResistance to tamoxifen is a major clinical challenge. Research in recent years has identified epigenetic changes as mediated by dysregulated miRNAs that can possibly play a role in resistance to tamoxifen in breast cancer patients expressing estrogen receptor (ER). We report here elevated levels of EMT markers (vimentin and ZEB1/2) and reduced levels of EMT-regulating miR-200 (miR-200b and miR-200c) in ER-positive breast cancer cells, MCF-7, that were resistant to tamoxifen, in contrast with the naïve parental MCF-7 cells that were sensitive to tamoxifen. Further, we established regulation of c-MYB by miR-200 in our experimental model. C-MYB was up-regulated in tamoxifen resistant cells and its silencing significantly decreased resistance to tamoxifen and the EMT markers. Forced over-expression of miR-200b/c reduced c-MYB whereas reduced expression of miR-200b/c resulted in increased c-MYB We further confirmed the results in other ER-positive breast cancer cells T47D cells where forced over-expression of c-MYB resulted in induction of EMT and significantly increased resistance to tamoxifen. Thus, we identify a novel mechanism of tamoxifen resistance in breast tumor microenvironment that involves miR-200-MYB signaling.

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