scholarly journals Total Phenols, Identification of Active Compounds and Anticancer Activity of Salvia judaica Boiss against the breast Cancer Cell MDA-231

2021 ◽  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Essential Oil ◽  
Anticancer Activity ◽  
Breast Cancer Cell ◽  
Annexin V ◽  
Ethanol Extract ◽  
G1 Phase ◽  
Apoptotic Cells ◽  
Total Phenols

Salvia judaica is an annual herb from genus Salvia L.; the largest genera of Lamiaceae. It’s a medicinal plant prominent in pharmaceutical applications in many countries around the world. This study aimed to explore bioactive compounds likely to be responsible for the plant anticancer activity, and evaluate anticancer effects, after determining the total content of phenols in the ethanol extract and essential oil in this species. Ethanol extract (EE) and essential oil (EO) were prepared from dried aerial parts (leaves and the flower). GC-MS analysis of EO showed the presence of/43/ effective compounds in varying proportions, the major compounds were sesquiterpenes like delta-cadinene, alpha-Gurjunene, beta-humulene, and alpha-caryophyllene. This is the first study revealed that S.judaica is so rich in phenols which proceeded S.officinalis, noting the superiority of the EE over the EO samples in the total phenols. Anticancer properties of EE and EO of S. judaica against MDA-231 breast cancer cell line were studied -for the first time - by cell cycle analysis and Annexin V/PI apoptosis assay using Flow cytometry technique. Cells were treated with EE (0.001, 0.01, 0.02, 0.1mg/ml) and EO (0.005, 0.01, 0.02, 0.03, 0.04 mg/ml) at various concentrations for48 h. The results revealed that both EE and EO induced cell cycle arrest at G1-phase. Cells treated with EE and EO for 48h showed increasing the percentage of cells in G1-phase and decreasing the percentage of cells in S-phase with increasing concentration compared with untreated cells (control). Annexin V-FITC/PI assay confirmed that EO and EE were able to induce apoptosis. Cells treated with EOat (0.04 mg/ml) for 48h resulted in apoptotic cells at 96.68%, and necrotic cells at 0.12%, compared with untreated cells. On the other hand, Cells treated with EE at (0.1 mg/ml) for 48h resulted in apoptotic cells at 94.43%, and necrotic cells at 0.47%, compared with control. Results revealed that EO is better than EE as anticancer; treatment with EO resulted in more apoptotic cells and less necrotic cells, and there were significant differences between them. This confirmed that EO contains specific anticancer compounds as showed by GC-MS analysis. However, more studies should be performed to explore antioxidants present in S.judaica and determine the underlying mechanism of their anti-breast cancer properties.

scholarly journals Growth factor, steroid, and steroid antagonist regulation of cyclin gene expression associated with changes in T-47D human breast cancer cell cycle progression.

1993 ◽  
Vol 13 (6) ◽  
pp. 3577-3587 ◽  
Author(s):  
E A Musgrove ◽  
J A Hamilton ◽  
C S Lee ◽  
K J Sweeney ◽  
C K Watts ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Cycle ◽  
Cyclin D1 ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Cycle Progression ◽  
S Phase ◽  
G1 Phase ◽  
Cycle Progression

Cyclins and proto-oncogenes including c-myc have been implicated in eukaryotic cell cycle control. The role of cyclins in steroidal regulation of cell proliferation is unknown, but a role for c-myc has been suggested. This study investigated the relationship between regulation of T-47D breast cancer cell cycle progression, particularly by steroids and their antagonists, and changes in the levels of expression of these genes. Sequential induction of cyclins D1 (early G1 phase), D3, E, A (late G1-early S phase), and B1 (G2 phase) was observed following insulin stimulation of cell cycle progression in serum-free medium. Transient acceleration of G1-phase cells by progestin was also accompanied by rapid induction of cyclin D1, apparent within 2 h. This early induction of cyclin D1 and the ability of delayed administration of antiprogestin to antagonize progestin-induced increases in both cyclin D1 mRNA and the proportion of cells in S phase support a central role for cyclin D1 in mediating the mitogenic response in T-47D cells. Compatible with this hypothesis, antiestrogen treatment reduced the expression of cyclin D1 approximately 8 h before changes in cell cycle phase distribution accompanying growth inhibition. In the absence of progestin, antiprogestin treatment inhibited T-47D cell cycle progression but in contrast did not decrease cyclin D1 expression. Thus, changes in cyclin D1 gene expression are often, but not invariably, associated with changes in the rate of T-47D breast cancer cell cycle progression. However, both antiestrogen and antiprogestin depleted c-myc mRNA by > 80% within 2 h. These data suggest the involvement of both cyclin D1 and c-myc in the steroidal control of breast cancer cell cycle progression.

scholarly journals Peptide SA12 inhibits proliferation of breast cancer cell lines MCF-7 and MDA-MB-231 through G0/G1 phase cell-cycle arrest

2018 ◽  
Vol Volume 11 ◽  
pp. 2409-2417 ◽  
Author(s):  
Longfei Yang ◽  
Huanran Liu ◽  
Min Long ◽  
Xi Wang ◽  
Fang Lin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Phase Cell ◽  
G1 Phase ◽  
Breast Cancer Cell Lines ◽  
Cycle Arrest ◽  
Mcf 7

Growth factor, steroid, and steroid antagonist regulation of cyclin gene expression associated with changes in T-47D human breast cancer cell cycle progression

1993 ◽  
Vol 13 (6) ◽  
pp. 3577-3587
Author(s):  
E A Musgrove ◽  
J A Hamilton ◽  
C S Lee ◽  
K J Sweeney ◽  
C K Watts ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Cycle ◽  
Cyclin D1 ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Cycle Progression ◽  
S Phase ◽  
G1 Phase ◽  
Cycle Progression

Cyclins and proto-oncogenes including c-myc have been implicated in eukaryotic cell cycle control. The role of cyclins in steroidal regulation of cell proliferation is unknown, but a role for c-myc has been suggested. This study investigated the relationship between regulation of T-47D breast cancer cell cycle progression, particularly by steroids and their antagonists, and changes in the levels of expression of these genes. Sequential induction of cyclins D1 (early G1 phase), D3, E, A (late G1-early S phase), and B1 (G2 phase) was observed following insulin stimulation of cell cycle progression in serum-free medium. Transient acceleration of G1-phase cells by progestin was also accompanied by rapid induction of cyclin D1, apparent within 2 h. This early induction of cyclin D1 and the ability of delayed administration of antiprogestin to antagonize progestin-induced increases in both cyclin D1 mRNA and the proportion of cells in S phase support a central role for cyclin D1 in mediating the mitogenic response in T-47D cells. Compatible with this hypothesis, antiestrogen treatment reduced the expression of cyclin D1 approximately 8 h before changes in cell cycle phase distribution accompanying growth inhibition. In the absence of progestin, antiprogestin treatment inhibited T-47D cell cycle progression but in contrast did not decrease cyclin D1 expression. Thus, changes in cyclin D1 gene expression are often, but not invariably, associated with changes in the rate of T-47D breast cancer cell cycle progression. However, both antiestrogen and antiprogestin depleted c-myc mRNA by > 80% within 2 h. These data suggest the involvement of both cyclin D1 and c-myc in the steroidal control of breast cancer cell cycle progression.

Hyaluronan arrests human breast cancer cell growth by prolonging the G0/G1 phase of the cell cycle

2018 ◽  
Vol 50 (12) ◽  
pp. 1181-1189 ◽  
Author(s):  
Xiaoyan Chen ◽  
Yan Du ◽  
Yiwen Liu ◽  
Yiqing He ◽  
Guoliang Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Growth ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
G1 Phase ◽  
Human Breast ◽  
Cancer Cell Growth ◽  
Breast Cancer Cell Growth

scholarly journals A chemical screen in diverse breast cancer cell lines reveals genetic enhancers and suppressors of sensitivity to PI3K isoform-selective inhibition

2008 ◽  
Vol 415 (1) ◽  
pp. 97-110 ◽  
Author(s):  
Neil E. Torbett ◽  
Antonio Luna-Moran ◽  
Zachary A. Knight ◽  
Andrew Houk ◽  
Mark Moasser ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Cycle ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Therapeutics ◽  
Cancer Cell Lines ◽  
Genetic Alterations ◽  
Breast Cancer Cell Lines ◽  
Selective Inhibitors

The PI3K (phosphoinositide 3-kinase) pathway regulates cell proliferation, survival and migration and is consequently of great interest for targeted cancer therapy. Using a panel of small-molecule PI3K isoform-selective inhibitors in a diverse set of breast cancer cell lines, we have demonstrated that the biochemical and biological responses were highly variable and dependent on the genetic alterations present. p110α inhibitors were generally effective in inhibiting the phosphorylation of PKB (protein kinase B)/Akt and S6, two downstream components of PI3K signalling, in most cell lines examined. In contrast, p110β-selective inhibitors only reduced PKB/Akt phosphorylation in PTEN (phosphatase and tensin homologue deleted on chromosome 10) mutant cell lines, and was associated with a lesser decrease in S6 phosphorylation. PI3K inhibitors reduced cell viability by causing cell-cycle arrest in the G1 phase, with multi-targeted inhibitors causing the most potent effects. Cells expressing mutant Ras were resistant to the cell-cycle effects of PI3K inhibition, which could be reversed using inhibitors of Ras signalling pathways. Taken together, our data indicate that these compounds, alone or in suitable combinations, may be useful as breast cancer therapeutics, when used in appropriate genetic contexts.

scholarly journals Pharmacokinetic, Antiproliferative and Apoptotic Effects of Phenolic Acids in Human Colon Adenocarcinoma Cells Using In Vitro and In Silico Approaches

Molecules ◽  
2018 ◽  
Vol 23 (10) ◽  
pp. 2569 ◽  
Author(s):  
Lana Rosa ◽  
Nathállia Jordão ◽  
Nathália da Costa Pereira Soares ◽  
Joelma deMesquita ◽  
Mariana Monteiro ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Colon Cancer ◽  
Cell Viability ◽  
Colon Adenocarcinoma ◽  
Human Colon ◽  
G1 Phase ◽  
Apoptotic Cells ◽  
Adenocarcinoma Cells ◽  
Human Colon Adenocarcinoma ◽  
Colon Adenocarcinoma Cells

Colon cancer is the second most common cause of cancer deaths in the USA and Europe. Despite aggressive therapies, many tumors are resistant to current treatment protocols and epidemiological data suggest that diet is a major factor in the etiology of colon cancer. This study aimed to evaluate the antioxidant activity and the influence of 3,4-dihydroxyphenylacetic (3,4-DHPAA), p-coumaric (p-CoA), vanillic (VA) and ferulic (FA) acids on cell viability, cell cycle progression, and rate of apoptosis in human colon adenocarcinoma cells (HT-29). The results showed that all compounds tested reduce cell viability in human colon cancer cells. 3,4-DHPAA promoted the highest effect antiproliferative with an increase in the percentage of cells in G0/G1 phase, accompanied by a reduction of cells in G2/M phase. Cell cycle analysis of VA and FA showed a decrease in the proportion of cells in G0/G1 phase (10.0 µM and 100.0 µM). p-CoA and FA acids increased the percentage of apoptotic cells and non-apoptotic cells. 3,4-DHPAA seems to be the substance with the greatest potential for in vivo studies, opening thus a series of perspectives on the use of these compounds in the prevention and treatment of colon cancer.

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