جستجوی مقالات مرتبط با کلیدواژه « skbr3 cells » در نشریات گروه « پزشکی »

In recent years, nanotechnology has gained serious attention for diagnosis, prevention and treatment roles. In this study we synthesized nanoceria or CeO2NPs (cerium oxide nanoparticles) and compared toxicity of cerium oxide powder in nano and bulk forms in two cancerous and one normal cell lines. The cell lines were cultured in a standard humidified incubator, at 37 °C in a 5% CO2 atmosphere, in RPMI 1640 medium. The cells were incubated with different concentrations of cerium oxide (from 2 μg/mL to 64 μg/mL) in bulk and nano forms. To determine the effect of cerium oxide on cell viability after 24 h, 48 h, and 72 h incubation, a MTT assay was performed using SKBR3 (human breast cancer cell line), A431 (Human epidermoid carcinoma cell line) and C2Cl2 (ATCC mouse skeletal muscle cell line) cells. Analysis of variance followed by Sidak post-hoc test, shows the toxicity of nanoceria is significantly deferent from bulk form on three cell lines in this study and is more on cancerous cells in compared to normal cells especially in higher level of concentrations after 24, 48 and 72 hours (All P<0.05). Additionally, the effect of cell lines, cerium oxide forms and concentrations cerium oxide leads in significantly the lowest amount of viability after 72 hours compared with 24 hours and 48 hours.

Fatty acid synthase (FASN) is a key enzyme in de novo lipogenesis pathway. FASN overexpression is a common feature of many human cancers like breast cancer. Furthermore, FASN expression in HER2 - positive cell lines like SKBR3 is more than other cell lines, such as MCF - 7, which are not HER2 - positive. Cichorium intybus is a medicinal herb and methanolic extract of this plant significantly suppressed cell viability and growth in some cancer cells.
In this study, we aimed at investigating the effect of methanolic extract of Cichorium intybus on the FASN expression and, therefore, lipogenesis pathway in human breast cancer SKBR3 cell line.
We assessed the cytotoxicity effect of Chicorium intybus on the cell viability of SKBR3 cells, using MTT assay. In addition, apoptosis rate was assessed by annexinV/PI flow cytometry. Finally, Real time q - PCR was used for the analysis of FASN gene expression.
The results showed that the methanolic extract of Cichorium intybus caused a dose - dependent decrease in the cell viability of SKBR3 cells. Additionally, the treatment of confluent SKBR3 cells with extract led to reduced FASN expression at mRNA level.
These results suggest that Chicorium intybus not only inhibits cell viability in a dose - dependent manner, but also presumably inhibits lipogenesis by markedly decreased FASN expression as a key lipogenic enzyme.

The poor prognosis of breast cancer is due to its resistance to the conventional treatments. Therefore, researchers are studying about herbs which have anticancer effects. Emodin is a hydroxy-anthraquinone that is found in many medicinal plants and has biological and anticancer effects. According to previous studies, it inhibited the growth of cancer cells by apoptosis.
In this study, we aimed to determine the effect(s) of emodin on growth and proliferation of SKBR3 cancer cells.
SKBR3 cells were cultivated for 24 hours. Then different concentrations of emodin (0, 10, 25 and 50 µM) were added to the test wells and incubated for 24, 48 and 72 hours. Cell viability was examined by MTT assay after 24, 48 and 72 hours. Apoptosis was determined in cells treated with emodin (0, 10, 25 and 50 µM) using flow cytometric assay. Alterations in expression of apoptotic-related genes (Caspase 3, 8, 9, Bcl2 and Bax) were determined by real time PCR. Caspase 3 activity was measured using a colorimetric assay.
Emodin had inhibitory effects on the proliferation of SKBR3 cells with IC50 value of 25 µM. Emodin induced apoptosis and increased the mRNA expression of Caspase 3, 8, 9 and Bax and decreased the mRNA expression of Bcl2 in SKBR3 cells. It also increased the activity of Caspase 3.
Emodin had an inhibitory effect on the growth of SKBR3 cell line in a dose and time dependent manner. This study indicated that emodin induces apoptosis in SKBR3 cells through the alterations of the expression of apoptosis-related genes and increases the activity of Caspase 3.