Effects of the Gold Nanoparticles (AuNPs) on the Proliferation and Morphological Characteristics of Human Breast Cancer Cells (MCF-7) in Culture

2017 ◽  
Vol 268 ◽  
pp. 254-258 ◽  
Author(s):  
Nur Shafawati Rosli ◽  
Azhar Abdul Rahman ◽  
Azlan Abdul Aziz ◽  
Shaharum Shamsuddin ◽  
Nurul Sabihah Zakaria

Ultrastructural characteristic and morphological changes of untreated and treated breast cancer MCF-7 cells were observed by energy-filtered transmission electron microscope (EFTEM). Morphological observation of MCF-7 after being treated with 13 nm, 50 nm, and 70 nm AuNPs, were looking unhealthy and dying out of the populace, the observed cells were more reduced and dying as treatment with 50 nm and 70 nm AuNPs. Cells detachment, clumping, shrunken, and dispersed cells in the culture medium and floating cells were also observed. The observed morphological changes increase in 50 nm and 70 nm AuNPs than in 13 nm AuNPs, which is less toxic to MCF-7 cells. The presented morphological analysis has established that 13 nm AuNPs showed less toxic to MCF-7 breast cancer cells. Whereas, control cells of MCF-7 were treated with only complete culture media, despite the duration of treatment, whereby the cells maintained most of their morphological features and observed to have a typical morphology of healthy cells that are well attached to the surface. These results indicate that AuNPs were clustered in the cells and there was no significant difference between images of different sizes of AuNPs observed in the cells, because the AuNPs always clustered together inside the cells.

2019 ◽  
Vol 15 (7) ◽  
pp. 745-751 ◽  
Author(s):  
Stefania D'Angelo ◽  
Elisa Martino ◽  
Giovanna Cacciapuoti

Background: Dietary micronutrients have been proposed as effective inhibitory agents for cancer initiation, progression, and incidence. Among them, polyphenols, present in different foods and beverages, have retained attention in recent years. Apples are among the most consumed fruits worldwide, and several studies suggest that apple polyphenols could play a role in the prevention of degenerative diseases. Aims and Objectives: The present study aimed at evaluating the effects of Annurca flesh polyphenols extract (AFPE) effects of proliferation on MCF-7 cells. Methods: The data indicated that apple polyphenolic compounds had a significant antiproliferative action on MCF-7 cells and 500μM EqC AFPE induced a cell cycle arrest at G2/M. AFPE was also capable of inducing morphological changes as evidenced by nuclear condensation. Results: The cellular, morphological, and molecular data unequivocally suggested that induction of cellular apoptosis was mainly responsible for the previously observed antiproliferation-induced AFPE on MCF-7 cells. Conclusion: Taken together, AFPE that acts at a low micromolar range against breast cancer cells may be considered as a promising candidate for anticancer therapy.


YMER Digital ◽  
2021 ◽  
Vol 20 (12) ◽  
pp. 385-396
Author(s):  
Sumathi R ◽  
◽  
Sivagamasundari K ◽  

The present work demonstrates the influence of plant extract composition (antioxidant and total phenolic content) on the size and morphology of the produced AgNPs. In this study, silver nanoparticles (AgNPs) were synthesized using aqueous flower extract of Allamanda neriifolia plant. The biosynthetic procedure was rapid and simple and was easily monitored via colour changes and examined AgNPs (AN-AgNPs) by ultraviolet-visible spectroscopy, Fourier transform infrared (FTIR) spectroscopy and scanning electron microscope (SEM). The results obtained from various characterizations revealed that average size of synthesized AgNPs was 50 nm and in spherical structure. The anticancer potential of AN-AgNPs was investigated against human breast cancer cells (MCF-7). The cytotoxic response was assessed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT), and morphological changes by apoptosis. The biosynthesized AgNPs-induced cell death in MCF- 7 cells suggested the anticancer potential of AN-AgNPs. Therefore, they may be used to treat the breast cancer cells.


2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e12540-e12540
Author(s):  
Tae Hyun Kim ◽  
In-Sung Song ◽  
Jin Han

e12540 Background: Breast cancer is the most common non-skin cancer in women. Breast cancers are heterogeneous, and treatment by subgroup based on hormone receptor and HER2 made a significant difference in clinical outcomes. Several studies have reported that estrogen receptor beta (ERβ) decreases during tumor development in the breast epithelium. However, the role of ERβ in relapse and metastasis of breast cancer is poorly understood. Methods: In this study, we retrospectively studied 30 case breast carcinomas divided luminal, HER2, and triple negative subtype. Among them, patients relapsed within 5 years are 6 cases. The expression of ERβ gene in breast cancer tissues (30 cases) was estimated using a quantitative PCR, and other marker (ERα, HER2, PR etc) was measured anonymously in formalin-fixed paraffin-embedded tumor sections, by using specific antibodies. Results: A low level of ERβ expression and mitochondrial translocation of ERβ was associated with relapse/metastasis of breast cancer. The ERβ depletion resulted in resistance in response to tamoxifen treatment of MCF-7 breast cancer cells. Conversely, the overexpression of mitochondrial ERβ enhanced the cell death by treatment of tamoxifen in MCF-7 cells. We found that ERβ localizes to the mitochondria via the interaction with Grp75 and improves mitochondrial oxygen consumption rate and ATP production in breast cancer cells. Finally, we showed that ERβ level was a low in the breast cancer stem cells (CD24-CD44+ cells) compared with breast non-cancer stem cells (CD24+CD44- cells), whereas ERα level was a high. The overexpression of mitochondrial ERβ contribute to a decrease of sphere formation showing a tumorigenic ability. Conclusions: The mitochondrial ERβ contribute to suppress survival and stemness of cancer stem cells for relapse/metastasis, promising to the development of novel strategies for the treatment of breast cancer patients.


2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15592-e15592
Author(s):  
Yan Kong ◽  
Qian Dong ◽  
Cuizhi Geng ◽  
Da Jiang

e15592 Background: To investigate the effect and mechanism of IKKβ on proliferation, apoptosis, invasion and metastasis of breast cancer cells with different expression levels of leptin and ObR. Methods: IKKβ in breast cancer cells was knocked down via virus transfection technology. MTT, flow cytometry, cell scratch test and clone formation test were used to observe the effect of IKKβ on proliferation, apoptosis and metastasis of breast cancer cells with different expression levels of leptin and ObR. RT-PCR was used to detect the downstream genes expressions in IKKβ signaling pathway. Results: The expression levels of leptin and ObR in MDA-MB-231 cells were higher than those in MCF-7 cells. Lentivirus can successfully infect breast cancer cells in vitro and knock down the expression of IKKβ. Knocking down IKKβ reduced the viability of MDA-MB-231 cells, but had little effect on MCF-7, and had an effect on the cell cycle of both cells. After knocking down IKKβ, the apoptotic rate of MDA-MB-231 cells increased. There was no significant difference in the apoptotic rate of MCF-7 cells. The number of clones of MCF-7 and MDA-MB-231 cells decreased, and the difference was significant. The effect on MDA-MB-231 cells was more significant. The scratch mobility of MDA-MB-231 cells decreased significantly, with significant difference.After knocking down IKKβ, the expressions of leptin and ObR, IKBKG, P65 and HIF in MCF-7 cells were significantly decreased, and there was statistical significance. However, the above indicators were significantly increased in MDA-MB-231 cells. The expression level of IKBKG was increased significantly, whereas that of HIF did not differ significantly, as compared with that of control group. Conclusions: The proliferation, metastasis and apoptosis of MDA-MB-231 cells were inhibited after blocking the IKKβ pathway, while the proliferation of MCF-7 cells was inhibited, and the apoptosis did not change significantly. The difference between the two cells may be related to the different expression levels of leptin and ObR.After blocking the IKKβ signaling pathway, the expressions of genes related to the IKKβ signaling pathway in MDA-MB-231 cells were increased, whereas those in MCF-7 cells were decreased, which might be related to the different expression levels of leptin and ObR.After knocking down IKKβ, the expressions of HIF gene in MCF-7 cells were decreased, whereas those in MDA-MB-231 cell lines were not affected. It needs to be verified whether this difference is related to leptin and ObR.


2021 ◽  
Vol 11 ◽  
Author(s):  
Eun-Young Kim ◽  
Ji-Eun Kim ◽  
Bongkun Choi ◽  
Jiyeon Kweon ◽  
Si-On Park ◽  
...  

TNF-α plays a crucial role in cancer initiation and progression by enhancing cancer cell proliferation, survival, and migration. Even though the known functional role of AWP1 (zinc finger AN1 type-6, ZFAND6) is as a key mediator of TNF-α signaling, its potential role in the TNF-α-dependent responses of cancer cells remains unclear. In our current study, we found that an AWP1 knockdown using short hairpin RNAs increases the migratory potential of non-aggressive MCF-7 breast cancer cells with no significant alteration of their proliferation in response to TNF-α. A CRISPR/Cas9-mediated AWP1 knockout in MCF-7 cells led to mesenchymal cell type morphological changes and an accelerated motility. TNF-α administration further increased this migratory capacity of these AWP1-depleted cells through the activation of NF-κB accompanied by increased epithelial-mesenchymal transition-related gene expression. In particular, an AWP1 depletion augmented the expression of Nox1, reactive oxygen species (ROS) generating enzymes, and ROS levels and subsequently promoted the migratory potential of MCF-7 cells mediated by TNF-α. These TNF-α-mediated increases in the chemotactic migration of AWP1 knockout cells were completely abrogated by an NF-κB inhibitor and a ROS scavenger. Our results suggest that a loss-of-function of AWP1 alters the TNF-α response of non-aggressive breast cancer cells by potentiating ROS-dependent NF-κB activation.


Author(s):  
Ileana MICLEA ◽  
Ana-Maria PUI ◽  
Marius ZĂHAN

Morphine, a highly potent analgesic, is prescribed for the treatment of severe pain associated with cancer. Several in vitro and animal studies suggest that morphine is involved both in promoting and inhibiting tumor growth. Our aim was to test the outcome of adding morphine to the culture media of cells from two of the most widely used breast cancer cell lines. MCF-7 and T47D cells were seeded into 96-well microplates and cultured for 24 hours in MEM and RPMI-1640 media respectively. Afterwards, cells were exposed for 24, 48 or 72 hours to media containing morphine at the following concentrations: 0.05, 0.075, 0.1, 0.25, 0.5, 0.75, 1 μM. Cell viability was assessed by the MTT colorimetric method. After exposure of MCF-7 cells to morphine for 24 and 48 hours, viability was similar to the control while, after 72 hours, this parameter was significantly enhanced at 0.75 μM and 1 μM. Survival of T47D cells in the first 24 hours was significantly (p<0.05) increased by the presence of 1 μM morphine, while an increased exposure time did not improve the outcome. Our results show that morphine can increase viability of breast cancer cells, depending on concentration, exposure time and cell origin.


Sign in / Sign up

Export Citation Format

Share Document