جستجوی مقالات مرتبط با کلیدواژه « MCF-7 cells » در نشریات گروه « پزشکی »

 Cancer, the second leading cause of mortality worldwide, represents a global health challenge, primarily due to drug resistance. Vinorelbine is a chemotherapeutic agent that disrupts cancer cell growth by targeting microtubules and inducing apoptosis. However, drug resistance remains a formidable obstacle. This resistance is caused by various factors including genetic mutations, drug efflux mechanisms, and DNA repair systems. Resolution of this challenge requires an innovative approach. This study investigated the potential of small interfering RNA (siRNA) to target and downregulate a vinorelbine-resistant MCF-7/ADR breast cancer cell line.

 Cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) 10% fetal bovine serum/penicillin/streptomycin. An siRNA targeting ABCB1 was designed and synthesized, and the cells were transfected with siRNA at final concentrations of 10, 20, and 30 nM. The3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was used to assess cell viability. ABCB1 mRNA expression levels were determined by real-time polymerase chain reaction (PCR).

 MCF-7 cells exhibited a higher sensitivity to vinorelbine than MCF-7/ADR cells. MCF-7/ADR cells exhibited resistance to vinorelbine at concentrations, 12.50 and 25.00 μM. Treatment with siRNA significantly reduced ABCB1 expression by 2.93-fold (P=0.0001). Similarly, co-treatment with siRNA and vinorelbine produced a substantial 2.89-fold decrease in ABCB1 gene expression in MCF-7 cells compared to that in MCF-7/ADR cells (P=0.0001).

 The results of the present study indicate that the concurrent use of siRNA and vinorelbine holds substantial promise as a therapeutic approach to overcome ABCB1-mediated multidrug resistance (MDR) in breast cancer. It is necessary to conduct comprehensive clinical trials to determine the true effectiveness of this combination therapy.

Multi-drug resistance is an important challenge in the chemotherapy of cancer. The role of annexin A5 (ANXA5) in the biology of cancer has been the focus of many studies. Breast Cancer (BC) is frequent cancer in women with high morbidity and mortality rate. The present study aimed to investigate the effects of ANXA5 overexpression on the anti-tumor activity of Epirubicin (EPI) in MCF-7 and MCF-7/ADR cells.

MCF-7 and MCF-7/ADR cells were transfected with the pAdenoVator- CMV-ANXA5-IRES-GFP plasmid or mock plasmid. The overexpression of ANXA5 was evaluated using qPCR. The effects of ANXA5 overexpression and EPI on the cell viability of MCF-7 and MCF-7/ADR cells were measured using an MTT assay. Cell apoptosis was measured by annexin V/7-AAD flow cytometry assay.

Following the overexpression of ANXA5, the viability of MCF-7 and MCF- 7/ADR was significantly decreased. Furthermore, the overexpression of ANXA5 in MCF-7 cells increased the cytotoxic effects of EPI in all doses and reduced the IC50 of EPI from 17.69 μM to 4.07 μM. Similarly, the overexpression of ANXA5 in MCF7- ADR cells reduced the IC50 of EPI from 27.3 μM to 6.69 μM. ANXA5 overexpression alone or combined with EPI treatment increased the apoptosis of MCF7 and MCF7- ADR cells.

The results of the present study demonstrate that ANXA5 overexpression increases the sensitivity of MCF-7 and MCF-7/ADR to EPI, suggesting a possible beneficial role of ANXA5 in the therapy of BC.

Discovering new cytotoxic compounds has received significant attention due to the rise in drug resistance and the adverse effects associated with chemotherapy drugs. In this study, the cytoplasmic extract of Lactobacillus casei was used to produce iron oxide nanoparticles (Fe2o3 NPs), and the cytotoxic effects of NPs were investigated on MCF-7 and human embryonic kidney 293 (HEK-293) cells.

The cytoplasmic extract of L. casei was mixed with 103M iron sulfate solution and incubated for 3 weeks at 37 °C and 5% CO2. The coprecipitation method was used to synthesize chemical Fe2o3 NPs. The synthesis of NPs was studied by electron microscopy and X-ray diffraction (XRD) analysis, and the cytotoxic effects were evaluated with dilutions (10, 100, and 1000 µg/mL) on MCF-7 and HEK cells.

X-ray diffraction analysis and scanning electron microscopy presented the mean of NPs synthesized by the green method to be about 15 nm and their shape to be spherical, as well as the average of chemically synthesized NPs to be about 20 nm with cubic structure. Chemical and green synthesized NPs only at a concentration of 1000 µg/mL were able to significantly reduce the survival rate of normal HEK-293 cells; chemically synthesized NPs decreased MCF-7 cell survival only at 1000 µg/mL and green synthesis at 100 µg/mL and 1000 µg/mL.

Generating Fe2o3 NPs is biologically safe using the green synthesis method and the cytoplasmic extract of L. casei, which may be a suitable candidate for the treatment of cancer cells.

Controlled drug delivery using nanotechnology enhances drug targeting at the site of interest and prevents drug dispersal throughout the body. This study focused on loading a poorly water-soluble drug Tamoxifen (TMX) into silica nanoparticles (SNPs) and amine-functionalized mesoporous silica nanoparticles (NH2-SBA-15).  SNPs were prepared according to the Stöber method and functionalized with an amine group using 3-aminopropyl triethoxysilane (APTES) through a one-pot synthesis method to produce amine-functionalized mesoporous silica nanoparticles (NH2-SBA-15). Characterization of both nanoparticles was performed using FT-IR, FE-SEM, CHN analysis, porosity tests (BET), and dynamic light scattering (DLS).  The results showed an average particle size of 103.7 nm for SNPs and 225.9 nm for NH2-SBA-15. Based on the BET results, the pore size of NH2-SBA-15 was about 5.4 nm. In both silica nanoparticles, drug release at pH=5.7 was greater than that of pH=7.4. However, Tamoxifen-loaded NH2-SBA-15 (TMX@NH2-SBA-15) indicated the highest drug release in the acidic medium among TMX-loaded SNPs (TMX@SNPs), perhaps due to the high columbic repulsion in the functionalized NH2-SBA-15 nanoparticles. Regarding cytotoxicity results against MCF-7 breast cancer cell lines, both TMX@SNPs and TMX@NH2-SBA-15 nanoparticles exhibited greater cytotoxicity compared to the free TMX as a positive control. Although TMX@SNPs had a small size and high loading capacity, the cytotoxic effects were higher than those of TMX@NH2-SBA-15. Amine functionalization of SNPs can improve the potential activity of these nanoparticles for target therapy.

 Breast cancer, as the most common malignancy among women, is shown to have a high mortality rate and resistance to chemotherapy. Research has shown the possible inhibitory role of Mesenchymal stem cells in curing cancer. Thus, the present work used human amniotic fluid mesenchymal stem cell-conditioned medium (hAFMSCs-CM) as an apoptotic reagent on the human MCF-7 breast cancer cell line.

 Conditioned medium (CM) was prepared from hAFMSCs. After treating MCF-7 cells with CM, a number of analytical procedures (MTT, real-time PCR, western blot, and flow cytometry) were recruited to evaluate the cell viability, Bax and Bcl-2 gene expression, P53 protein expression, and apoptosis, respectively. Human fibroblast cells (Hu02) were used as the negative control. In addition, an integrated approach to meta-analysis was performed.

 The MCF-7 cells’ viability was decreased significantly after 24 hours (P < 0.0001) and 72 hours (P < 0.05) of treatment. Compared with the control cells, Bax gene’s mRNA expression increased and Bcl-2’s mRNA expression decreased considerably after treating for 24 hours with 80% hAFMSCs-CM (P = 0.0012, P < 0.0001, respectively); an increasing pattern in P53 protein expression could also be observed. The flow cytometry analysis indicated apoptosis. Results from literature mining and the integrated meta-analysis showed that hAFMSCs-CM is able to activate a molecular network where Bcl2 downregulation stands in harmony with the upregulation of P53, EIF5A, DDB2, and Bax, leading to the activation of apoptosis.

 Our finding demonstrated that hAFMSCs-CM presents apoptotic effect on MCF-7 cells; therefore, the application of hAFMSCs-CM, as a therapeutic reagent, can suppress breast cancer cells’ viabilities and induce apoptosis.

Nanotechnology has helped a lot in diagnosing and treating multiple illnesses, specifically cancer, and increasing the development of targeted drug delivery methods. Nanocomposites are materials with at least one component smaller than 100 nm. Therefore, this study aims to assess the anticancer effects of silver-graphene nanocomposite on MCF-7. 

In this study, the rate of inhibition of cancer cell growth and production of reactive oxygen radicals, malondialdehyde, and glutathione stores in MCF7 cells were investigated. Cancer cells were exposed to nano particles for 48 hr. Silver nanoparticles and graphene both reduced the growth rate of MCF-7. 

Subsequently, by treating the cells with silver-graphene nanocomposite, the rate of inhibition of cell growth at the highest concentration was 84.60%. Nanoparticles also inhibited the growth of cancer cells through the oxidative stress pathway by increasing the amount of intracellular ROS, followed by increasing malondialdehyde and decreasing glutathione stores, so that at the highest combined concentration of nanoparticles, the amounts of LPO and ROS increased  up to 70% and 74 %, and glutathione reserves decreased by 16%. 

Treatment of MCF-7 cells with silver or graphene nanoparticles and combination treatment with these two substances against cisplatin have sound effects, and by affecting oxidative stress factors, such as increased ROS and subsequent increase in lipid membrane damage, inhibit cell growth and proliferation. According to the mathematical model, silver graphene nanocomposite> silver nanoparticles> graphene has the best effect in inhibiting the growth of cancer cells, respectively.

Chemotherapy, biotherapy, and radiotherapy play a limited but important role in treating breast cancer. For more efficient treatment, combination therapy could be an appropriate option. In this study, radiotherapy using neutron radiation emitted from a 241Am-Be neutron source, as well as biotherapy using curcumin (80 μM) was combined to investigate the efficiency of treatment towards MCF-7 breast cancer in a 3D culture medium.

MTT, NR uptake assay, NO, GSH assay, catalase, cytochrome c, comet assay, and caspase-3 were used to determine the effect of neutron radiation and also neutron and curcumin combination on the viability of cancer cells.

The results of cytotoxicity test showed that neutron irradiation with or without curcumin at 5, 10, 15, and 20 h reduced the survival of tumor cells. Moreover, the rate of apoptosis due to the neutron effect at different irradiation times enhanced with the increasing time.

Due to the significant anticancer effect of curcumin in 3D culture, using this molecule before or after neutron therapy is recommended.

Breast cancer cells produce exosomes that promote tumorigenesis. The anticancer properties of gallic acid have been reported. However, the mechanism underlying its anticancer effect on the exosomal secretory pathway is still unclear. We investigated the effect of gallic acid on exosome biogenesis in breast cancer cell lines.

The cytotoxic effect of gallic acid on MCF-10a, MCF-7, and MDA-MD-231 cells was measured by MTT assay after 48 hours treatment. Expression of miRNAs including miRNA-21, -155, and 182 as well as exosomal genes such as Rab27a, b, Rab11, Alix, and CD63; along with HSP-70 (autophagy gene), was determined using Q-PCR. The subcellular distribution of it was monitored by flow cytometry analysis. Isolated exosomes were characterized by transmission and scanning electron microscopes and flow cytometry. Acetylcholinesterase activity is used to measure the number of exosomes in supernatants. In addition, autophagy markers including LC3 and P62 were measured by ELISA.

Data showed that gallic acid was cytotoxic to cells (P < 0.05). Gallic acid modulated expression of miRNAs and down-regulated transcript levels of exosomal genes and up-regulated the HSP-70 gene in three cell lines (P < 0.05). The surface CD63/total CD63 ratio as well as acetylcholinesterase activity decreased in treated cells (P < 0.05). The protein level of LC3 was increased in three cell lines, while the expression of P62 increased in MCF-7 and MDA-MB-231 cancer cell lines.

Together, gallic acid decreased the activity of the exosomal secretory pathway in breast cancer cell lines, providing evidence for its anti-cancer effects.

Breast cancer is one of the most malignant cancersin the world. Cold micro plasma jet (CMPJ) Known as cold atmospheric jet microplasma, it has recently been introduced as an alternative way to overcome the challenges of finding an effective cancer treatment. Numerous studies have reported promising results, so our aim of this study was to investigate how this method affects cell death and its role on the expression of apoptotic genes in the MCF-7 cancer cell line.

In this study, helium gas was used to generate plasma at room temperature in the form of point radiation at different times of 30, 60, 90 and 120 seconds and at different distances of 1 cm. Flow cytometry will be used to examine the extent of apoptosis andnecrosis. Genes involved in apoptosis P53, P21, Bax and Bcl-2 were measured by real-time PCR.

Our Studie indicate that the mechanism of action of cold plasma on cancer cells is related to generation of reactive oxygen species with possible induction of the apoptosis pathway. The percentages of necrotic and late apoptotic cells following treatment with different times plasma (0, 30, 60, 90 and 120 s) were about 0.55 ± 0.06, 20.13 ± 0.01, 20.12 ± 0.03, 26.81 ± 0.04 and 17.51 ± 0.05. The mRNA expression of bcl-2 showed a decrease of 90s of plasma while the mRNA expression of p53, bax and caspase-8 genes increased compared to untreated cells.

In general, research in the last decade has confirmed the ability of CMPJ as an effective anti-cancer tool. Therefore, it may be used to help treat cancer. However, its clinical application requires much further studies to determine the severity and duration of exposure to CMPJ for effective treatment based on the type of cancer.

Recently, there is a significant focus on combination chemotherapy for cancer using a cytotoxic drug and a phytochemical compound. We investigated the effect of silibinin on etoposide-induced apoptosis in MCF-7 and MDA-MB-231 breast carcinoma cell lines. The cytotoxic effects of silibinin and etoposide were determined using MTT assay after 24 and 48 hr incubation with these drugs individually and combined. The mRNA expression of Bax and Bcl2, and protein levels of P53, phosphorylated p53 (P-P53), and P21 were determined using real-time PCR and western blot analysis, respectively. The caspase 9 activity was measured using an ELISA kit. Silibinin and etoposide alone and combined significantly inhibit cell growth in a dose and time-dependent manner in both cell lines. The strongest synergistic effects in terms of MCF-7 cell growth inhibition [combination index (CI) = 0.066] were evident. The silibinin-etoposide combinations cause a much powerful apoptotic death (47% and 40%) compared with each compound individually in MCF-7 and MDA-MB 231 cells, respectively. Additionally, the silibinin-etoposide combinations significantly increased the expression of P53, P-P53, and P21 in MCF-7 cells. Neither silibinin nor etoposide individually increased the level of P53 and P-P53 in MDA-MB-231 cells, but both of them individually and combined increased the level of P21. Since the silibinin-etoposide combination induces apoptosis in both cell lines with and without expression of p53, thus, it is suggested that this combination may be a successful therapeutic strategy for breast cancer regardless of P53 status.

One of the most prevalent malignancies, which have severe effects on women's health, is breast cancer. Quercetin, a flavonoid found in vegetables, tea, and fruits, is known to have bioactive properties, such as anti-inflammatory, anti-oxidant, as well as anti-cancer. Long non-coding RNAs (lncRNAs) have been recognized to function as primary regulators of diverse cellular processes, including differentiation, development, and cell fate. INXS and UCA1 are lncRNAs that are upregulated and downregulated, respectively in cancer cells. This research aimed to assess the impact of quercetin on the expression of INXS and UCA1 genes in MCF-7 cells. Various quercetin concentrations at different times were used to treat MCF-7 cells. The cell viability and IC50 values were determined using MTT assay. Then, MCF-7 cells were incubated with various quercetin concentrations for 24, 48, and 72 h. Cell cycle analyzes were evaluated by flow cytometry. The levels of INXS and UCA1 genes expression compared with the GAPDH gene at different concentrations of quercetin were quantified using real-time PCR method. Based on the results, quercetin exerted a dose- and time-dependent inhibitory impact on the viability of MCF-7 cells. Furthermore, quercetin induced cell cycle arrest at the G2 phase in MCF-7 cells. Also, quercetin induced INXS upregulation and UCA1 downregulation in the MCF-7 cell line. These data suggest that quercetin might increase cell death by upregulating INXS and downregulating UCA1 lncRNAs in MCF-7 cells.

Nowadays, the prevalence of nicotine abuse among women has increased dramatically. In the current study, we aimed to investigate the effect of nicotine exposure on breast MCF-7 and ovarian OVCAR-3 cell lines for assessing the toxicity of nicotine in the cells of these organs.

The MCF-7 and OVCAR-3 cells were treated with increasing nicotine concentrations ranging from 0 (control), 10-11, 10-8 and 10-6 M for 24h. Effect of nicotine treatments on major antioxidant enzymes catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), cellular levels of glutathione (GSH) and malondialdehyde (MDA) were monitored.

We showed that the CAT activity in MCF-7 cells increased only at 10-6 M dose of nicotine. The GPx and GR activity was decreased at 10-8 and 10-6 M of nicotine in MCF-7 cells, but in OVCAR-3 cells, this decrease was significant only at 10-6 M dose of nicotine. Reduced GSH decrease was statistically significant only at 10-8 and 10-6 M of nicotine in MCF-7 cells; otherwise, in OVCAR-3 cells, this decline was significant only at 10-6 M of nicotine. Nicotine at 10-8 and 10-6 M concentration caused a significant increase in MDA levels in MCF-7 cells.

This study showed that breast MCF-7 cells are more vulnerable than ovarian OVCAR-3 cells against nicotine-induced oxidative toxicity.

Oxidative stress plays a key role in breast carcinogenesis. Cyclo (L-Leu-L-Pro) (CLP) is a homodetic cyclic dipeptide with 2,5-diketopiperazine scaffold isolated from marine actinobacteria. This study aimed to evaluate the protective activity of CLP and linear - (L-Leu-L-Pro) (LP) from tert-butyl hydroperoxide (tBHP)-induced damage using normal breast epithelial cell line model (MCF-12A).

The cytoprotective activity was evaluated by detecting the changes in intracellular ROS, mitochondrial superoxide, hydroxyl radical, hydrogen peroxide, and lipid peroxidation detection assays as well as cytotoxic assays of MTT, LDH assays and phase contrast microscopy. Genoprotective activity was evaluated by (Apurinic/Apyrimidinic) AP site, alkaline Comet, and 8-hydroxy-2- deoxyguanosine assays.

The marine cyclic peptide, CLP, significantly protected MCF-12A cells by scavenging tBHPinduced intracellular ROS such as super oxide, hydroxyl radicals and hydrogen peroxide, and by reducing the cytotoxicity and genotoxicity effect compared to LP. Moreover, the results showed that CD151 gene silencing by shRNA significantly reduced the overexpression of CD151, tBHP-induced ROS generation, cytotoxicity and genotoxicity in MCF-12A cells. The overexpression of CD151 caused increased levels of cytochrome P450, but was reduced following the application of CD151shRNA and CLP which led to elevated levels of intracellular ROS.

In the present study we noticed that CD151 gene silencing by shRNA and treatment with CLP have similar effects on reducing the intracellular ROS. This study uncovers the protective activity of CLP against a CD151- mediated oxidative stress-induced cellular damage. Our observations suggest that the anti-stress and anti-inflammation properties of CLPmight have implications in cancer and are worth testing in cancer cell lines and tumor cells.

Insulin induces anti-cancer drugs resistance in tumor cells. However, the mechanism by which insulin induces its drug resistance effects is not clear. In the present study, the expression of miR-221 in insulin-treated MCF-7 cells in response to the anti-cancer drug doxorubicin, was investigated.

In this experimental study, cell viability was evaluated using MTT (3-[4,5 dimethylthiazol-2- yl]-2,5-diphenyl tetrazolium bromide) assay. The expression level of miR-221 was determined by real time polymerase chain reaction (RT-PCR). Furthermore, the expression of insulin receptor (IR) and cleaved caspase-3 protein was assessed by Western blotting.

The results showed that treatment of the MCF-7 cells with insulin reduced the anti-cancer effects of doxorubicin. Viability of naive and insulin-treated cells following doxorubicin (DOX) treatment was 62.9 ± 5.7% and 79 ± 7.2%, respectively. Furthermore, the expression of miR-221 in insulin-treated cells was significantly increased (2.6 ± 0.37-fold change) as compared with the control group. A significant decrease (26%) in the expression of caspase-3 protein and a significant increase (24%) in IR were observed in insulin-induced drug resistant MCF-7 cells as compared to the naive cells.

Together, the data showed a positive correlation between the expression of miR-221 and IR expression, but a negative correlation with caspase3 expression, in insulin-induced drug resistant MCF-7 breast cancer cells. This could suggest a new mechanism for the role of miR-221 in cancer drugs resistance induced by insulin.

Some recent studies have reported anti-tumor activity for Thymol, but the findings are inconsistent. This study aimed to investigate and compare Thymolchr('39')s effects on MCF-7 cancer cells and fibroblasts while treated with tert-Butyl hydroperoxide (t-BHP).

In the pre-treatment, MCF-7 and fibroblast cells were treated with various Thymol concentrations and incubated for 24 h. Then, t-BHP was added to a final concentration of 50 μM, and the cells were incubated for one h. In the post-treatment, cells were incubated first with 50 μM t-BHP for one h and then treated with Thymol. Cell viability was tested by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Thymolchr('39')s antioxidant capacity was measured by DPPH and FRAP assays, and lipid peroxidation levels were determined by the TBARS method.

The thymol effects were dose-dependent, and despite their antioxidant properties, at concentrations of 100 µg/ml or more, increased t-BHP toxicity and reduced cancer cell viability. MTT assay result showed that pre-treatment and post-treatment with Thymol for 24 hours effectively reduced MCF-7 and fibroblast cell viability compared with the untreated control group. Both pre- and post-treatment of Thymol, normal fibroblast cell viability was significantly greater than that of the MCF-7 cells.

Our finding showed that Thymol appears to be toxic to MCF-7 cells at lower concentrations than fibroblasts after 24 hours of incubation. Pre-treatment with Thymol neutralized the oxidative effect of t-BHP in fibroblasts but was toxic for MCF-7 cells.

Leptin and leptin receptor (Ob-R) are associated with worse prognosis, distant metastasis, and poor survival of breast cancer. We investigated the cytotoxic effect of silibinin and curcumin, individually and combined, on Ob-R expression in MCF-7 cells.

This study was performed from October 2017 to April 2018 at the Department of Clinical Biochemistry, School of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran. The cytotoxic effect of silibinin and curcumin, individually and combined, and their corresponding half-maximal inhibitory concentration (IC50) values were determined using the methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay. The cells were treated with different concentrations of silibinin (50-400 μM), curcumin (10-35 μM), and their combinations for 24 and 48 hours. The expression of Ob-R was measured using the Western blot analysis by treating the cells with different concentrations of curcumin (10-25 μM), silibinin (50-250 μM), and their respective combinations. The difference in mean cell viability between the groups was calculated using one-way ANOVA followed by Tukey’s post hoc test.

Silibinin and curcumin exerted time- and dose-dependent cytotoxic effect on MCF-7 cells. After treatment with silibinin, the IC50 values were about 250 and 50 μM at 24 and 48 hours, respectively. In terms of treatment with curcumin, the IC50 values were about 25 and 15 μM at 24 and 48 hours, respectively. Following treatment with silibinin, the Western blot analysis showed that Ob-R expression significantly decreased at 150 μM (P=0.031) and 200 μM (P=0.023) concentrations. Curcumin did not significantly decrease the Ob-R expression, however, the expression significantly decreased (P=0.004) when it was combined with silibinin.

The combination of silibinin and curcumin significantly reduced Ob-R expression in MCF-7 cells compared with their individual effects.