scholarly journals MiR-200c Sensitizes Breast Cancer Cells to Carboplatin Treatment by Decreasing MDR1 Expression

2021 ◽  
Author(s):  
Shiva Najjary ◽  
Sahar Safaee ◽  
Ahad Mokhtarzadeh ◽  
Mohammad Amini ◽  
Nadia Bolandi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
High Rate ◽  
Expression Level ◽  
Mcf7 Cells ◽  
Mdr1 Gene Expression ◽  
Mdr1 Expression ◽  
Functional Analyses ◽  
Resistance To Chemotherapy

Abstract Background: Breast cancer (BC) is one of the most common cancers worldwide and is associated with a high rate of cancer mortality in women. Resistance to chemotherapy is considered a significant problem and a major challenge for the treatment of patients with BC. miR-200c belongs to a family of miRNAs that act as tumor inhibitors. The expression level of miR-200c has been reported to be decreased in cancers, especially in BC. The increased miR-200c expression can be considered as a potent inhibitor of drug resistance and tumor progression. Methods and Results: The current study examined the effect of miR-200c on enhancing the BC cells' sensitivity to Carboplatin through targeting MDR1 expression. To perform functional analyses, mimic miR-200c transfected to MCF7 cells. Then, the viability of the cells was investigated via MTT assay. Finally, the expression of associated genes assessed using qRT-PCR. The results indicated that downregulation of miR-200c was occurred in MCF7 cells in comparison to control. Besides, restoring miR-200c expression by regulating the expression level of the apoptotic gene reduces the viability of cancer cells. Moreover, miR-200c increased the sensitivity of MCF7 cells to Carboplatin via reducing the MDR1 gene expression. Conclusions: This study provided valuable data showing that miR-200c enhances the effect of carboplatin as a clinically approved chemotherapeutic agent, and restoring its expression could be considered as a promising targeted adjuvant therapy for BC management.

scholarly journals Comparative effect of thermo/pH-responsive polymer-coated gold nanocages and hollow nanostars on chemo-photothermal therapy of breast cancer cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Asrin Pakravan ◽  
Mehdi Azizi ◽  
Fariborz Rahimi ◽  
Farhad Bani ◽  
Farideh Mahmoudzadeh ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Mtt Assay ◽  
Photothermal Therapy ◽  
Breast Cancer Cells ◽  
Covalent Attachment ◽  
Mcf7 Cells ◽  
Dapi Staining ◽  
Hemolysis Assay ◽  
Gold Nanocages

Abstract Background Combination chemo-photothermal therapy appears to be one of the next generations of cancer treatment. In this study hollow gold nanostars (HGNSs) and gold nanocages (GNCs) were synthesized and stabilized with thermo-pH-sensitive thiol-end capped ABC triblock copolymer poly(acrylic acid)-b-poly(N isopropylacrylamide)-b-poly (e-caprolactone)-SH; PAA-b-PNIPAAm-b-PCL-SH (GNSs@Pol). Doxorubicin (Dox) was conjugated to the GNSs@Pol nanostructures via ionic interaction, covalent attachment and hydrogen bonding (GNSs@Dox-Pol). The physicochemical characteristics of prepared GNSs@Pol and GNSs were assessed using dynamic light scattering (DLS), transmission electron microscopy (TEM) and zeta potential techniques. Cytocompatibility of the GNSs@Pol was studied by hemolysis assay and MTT assay. The chemo-photothermal therapy (PTT) potential of GNSs@Dox-Pol was compared on MCF7 cells using MTT assay, cell cycle, DAPI staining and Annexin-V apoptosis assay techniques. Results Cell internalization results showed an almost complete uptake of GNSs@Pol by MCF-7 cells in the first 3 h of treatment. The heat generation measurement results showed that both of GNSs have a potential for light to heat conversion (∆T = 23–27 ºC) and HGNSs demonstrated better efficiency than GNCs after 10-min exposure to NIR irradiation. Following chemo-photothermal treatment, the highest cell mortality (90%) and apoptotic effects (97% apoptosis) were observed in HGNSs@Dox-Pol received laser irradiation treatment group. Conclusions This work highlights the potential application of designed GNSs@Dox-Pol in a combinational chemo-PTT to treat breast cancer cells. Graphic abstract

scholarly journals Role of FoxO1 activation in MDR1 expression in adriamycin-resistant breast cancer cells

2008 ◽  
Vol 29 (9) ◽  
pp. 1837-1844 ◽  
Author(s):  
C.-Y. Han ◽  
K.-B. Cho ◽  
H.-S. Choi ◽  
H.-K. Han ◽  
K.-W. Kang
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Mdr1 Expression

scholarly journals Orai3 calcium channel and resistance to chemotherapy in breast cancer cells: the p53 connection

2018 ◽  
Vol 25 (4) ◽  
pp. 693-707 ◽  
Author(s):  
Jessy Hasna ◽  
Frédéric Hague ◽  
Lise Rodat-Despoix ◽  
Dirk Geerts ◽  
Catherine Leroy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Calcium Channel ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Resistance To Chemotherapy

scholarly journals Epinephrine Infiltration of Adipose Tissue Impacts MCF7 Breast Cancer Cells and Total Lipid Content

2019 ◽  
Vol 20 (22) ◽  
pp. 5626 ◽  
Author(s):  
Pierre Avril ◽  
Luciano Vidal ◽  
Sophie Barille-Nion ◽  
Louis-Romée Le Nail ◽  
Françoise Redini ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Tumor Progression ◽  
Cancer Cells ◽  
Conditioned Medium ◽  
Lipid Composition ◽  
Breast Cancer Cells ◽  
Quiescent State ◽  
Mcf7 Cells ◽  
Mesenchymal Transition

Background: Considering the positive or negative potential effects of adipocytes, depending on their lipid composition, on breast tumor progression, it is important to evaluate whether adipose tissue (AT) harvesting procedures, including epinephrine infiltration, may influence breast cancer progression. Methods: Culture medium conditioned with epinephrine-infiltrated adipose tissue was tested on human Michigan Cancer Foundation-7 (MCF7) breast cancer cells, cultured in monolayer or in oncospheres. Lipid composition was evaluated depending on epinephrine-infiltration for five patients. Epinephrine-infiltrated adipose tissue (EI-AT) or corresponding conditioned medium (EI-CM) were injected into orthotopic breast carcinoma induced in athymic mouse. Results: EI-CM significantly increased the proliferation rate of MCF7 cells Moreover EI-CM induced an output of the quiescent state of MCF7 cells, but it could be either an activator or inhibitor of the epithelial mesenchymal transition as indicated by gene expression changes. EI-CM presented a significantly higher lipid total weight compared with the conditioned medium obtained from non-infiltrated-AT of paired-patients. In vivo, neither the EI-CM or EI-AT injection significantly promoted MCF7-induced tumor growth. Conclusions: Even though conditioned media are widely used to mimic the secretome of cells or tissues, they may produce different effects on tumor progression, which may explain some of the discrepancy observed between in vitro, preclinical and clinical data using AT samples.

scholarly journals Identification of hub genes associated with RNAi-induced silencing of XIAP through targeted proteomics approach in MCF7 cells

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Mehdi Agha Gholizadeh ◽  
Fatemeh T. Shamsabadi ◽  
Ahad Yamchi ◽  
Masoud Golalipour ◽  
Gagan Deep Jhingan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Specific Antigen ◽  
Mapk Signaling ◽  
2D Electrophoresis ◽  
Mcf7 Cells ◽  
Apoptosis Pathway ◽  
Apoptosis Protein ◽  
Mcf 7

Abstract Background The X-linked inhibitor of apoptosis protein (XIAP) is the most potent caspase inhibitor of the IAP family in apoptosis pathway. This study aims to identify the molecular targets of XIAP in human breast cancer cells exposed to XIAP siRNA by proteomics screening. The expression of XIAP was reduced in MCF-7 breast cancer cells by siRNA. Cell viability and the mRNA expression level of this gene were evaluated by MTS and quantitative real-time PCR procedures, respectively. Subsequently, the XIAP protein level was visualized by Western blotting and analyzed by two-dimensional (2D) electrophoresis and LC–ESI–MS/MS. Results Following XIAP silencing, cell proliferation was reduced in XIAP siRNA transfected cells. The mRNA transcription and protein expression of XIAP were decreased in cells exposed to XIAP siRNA than si-NEG. We identified 30 proteins that were regulated by XIAP, of which 27 down-regulated and 3 up-regulated. The most down-regulated proteins belonged to the Heat Shock Proteins family. They participate in cancer related processes including apoptosis and MAPK signaling pathway. Reduced expression of HSP90B1 was associated with apoptosis induction by androgen receptor and prostate specific antigen. Suppression of XIAP resulted in the enhancement of GDIB, ENO1, and CH60 proteins expression. The network analysis of XIAP-regulated proteins identified HSPA8, HSP90AA1, ENO1, and HSPA9 as key nodes in terms of degree and betweenness centrality methods. Conclusions These results suggested that XIAP may have a number of biological functions in a diverse set of non-apoptotic signaling pathways and may provide an insight into the biomedical significance of XIAP over-expression in MCF-7 cells.

scholarly journals FRA-1 expression level regulates proliferation and invasiveness of breast cancer cells

Oncogene ◽  
2004 ◽  
Vol 24 (8) ◽  
pp. 1434-1444 ◽  
Author(s):  
Karine Belguise ◽  
Nathalie Kersual ◽  
Florence Galtier ◽  
Dany Chalbos
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Expression Level

scholarly journals Trametenolic Acid B Reverses Multidrug Resistance in Breast Cancer Cells Through Regulating the Expression Level of P-Glycoprotein

2013 ◽  
Vol 28 (7) ◽  
pp. 1037-1044 ◽  
Author(s):  
Qiaoyin Zhang ◽  
Junzhi Wang ◽  
Haibo He ◽  
Hongbing Liu ◽  
Ximing Yan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Multidrug Resistance ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Expression Level ◽  
P Glycoprotein

scholarly journals LAMP3 is involved in tamoxifen resistance in breast cancer cells through the modulation of autophagy

2014 ◽  
Vol 21 (1) ◽  
pp. 101-112 ◽  
Author(s):  
Anika Nagelkerke ◽  
Anieta M Sieuwerts ◽  
Johan Bussink ◽  
Fred C G J Sweep ◽  
Maxime P Look ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tamoxifen Resistance ◽  
Tamoxifen Treatment ◽  
Breast Cancer Patients ◽  
Mcf7 Cells ◽  
First Line ◽  
Tamoxifen Resistant

Lysosome-associated membrane protein 3 (LAMP3) is a member of the LAMP-family of proteins, which are involved in the process of autophagy. Autophagy is induced by tamoxifen in breast cancer cells and may contribute to tamoxifen resistance. In this study, the significance of LAMP3 for tamoxifen resistance in breast cancer was examined. The methods employed included use of clonogenic assays to assess the survival of MCF7 breast cancer cells with LAMP3 knockdown after tamoxifen treatment and of quantitative real-time PCR of LAMP3 to evaluate its predictive value for first-line tamoxifen treatment in patients with advanced breast cancer. Results show that tamoxifen treatment of MCF7 cells induced LAMP3 mRNA expression. LAMP3 knockdown in these cells increased tamoxifen sensitivity. Evaluation of expression of the autophagy markers, LC3B and p62, after LAMP3 knockdown showed increased expression levels, indicating that cells with LAMP3 knockdown have a suppressed ability to complete the autophagic process. In addition, knockdown of autophagy-associated genes resulted in sensitization to tamoxifen. Next, tamoxifen-resistant MCF7 cells were cultured. These cells had a sevenfold higher LAMP3 mRNA expression, showed elevated basal autophagy levels, and could be significantly resensitized to tamoxifen by LAMP3 knockdown. In patients treated with first-line tamoxifen for advanced disease (n=304), high LAMP3 mRNA expression was associated with shorter progression-free survival (P=0.003) and shorter post-relapse overall survival (P=0.040), also in multivariate analysis. Together, these results indicate that LAMP3 contributes to tamoxifen resistance in breast cancer. Tamoxifen-resistant cells are resensitized to tamoxifen by the knockdown of LAMP3. Therefore, LAMP3 may be clinically relevant to countering tamoxifen resistance in breast cancer patients.

scholarly journals Expression of genes modulated by epigallocatechin-3-gallate in breast cancer cells

2018 ◽  
Vol 64 (3) ◽  
pp. 31-37
Author(s):  
Anna Bogacz ◽  
Marlena Wolek ◽  
Bogna Juskowiak ◽  
Monika Karasiewicz ◽  
Adam Kamiński ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adjuvant Therapy ◽  
Mrna Expression ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Molecular Mechanisms ◽  
Mrna Level ◽  
Expression Level ◽  
Mrna Levels ◽  
Mrna Expression Level

Summary Introduction: Breast cancer is the most common malignant cancer among women. Both drug resistance and metastasis are major problems in the treatment of breast cancer. Therefore, adjuvant therapy may improve patients’ survival and affect their quality of life. It is suggested that epigallocatechin gallate (EGCG) which is well known for its chemopreventive activity and acts on numerous molecular targets may inhibit the growth and metastasis of some cancers. Hence, discovering the metastatic molecular mechanisms for breast cancer may be useful for therapy. Objective: The aim of the study was to determine the effect of EGGC on the mRNA expression level of genes such as ZEB1, ABCB1, MDM2, TWIST1 and PTEN in MCF-7 breast cancer cells. Methods: MCF7/DOX were cultured in the presence of 0.2 μM DOX and EGCG (20-50 μM). The mRNA expression level was determined by real-time quantitative PCR using RealTime ready Custom Panel 96 kit. Results: Our results showed an important increase (about 2-fold for 20 μM EGCG + 0.2 μM DOX and 2.5-fold for 50 μM EGCG + 0.2 μM DOX, p<0.05) in ZEB1 expression levels. In case of ABCB1 gene lack of influence on the mRNA level was observed (p>0.05). We also observed significant decrease of ZEB1 expression in MCF7 cells with 20 μM and 50 μM EGCG (p<0.05). In addition, EGCG (20 μM) caused an increase of MDM2 and PTEN mRNA levels in almost 100% (p<0.05) and 40% (p>0.05), respectively. Lack of the influence of EGCG was noted for the TWIST1 gene expression. In case of MCF7/DOX we showed an increase of mRNA level of PTEN gene about 50% (p<0.05). Conclusions: These results suggest that EGCG may be potentially used in adjuvant therapy in the breast cancer treatment.

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