The Chemopreventive Effect of Tanacetum Polycephalum Against LA7-Induced Breast Cancer in Rats and the Apoptotic Effect of a Cytotoxic Sesquiterpene Lactone in MCF7 Cells: A Bioassay-Guided Approach

Karimian, Hamed; Fadaeinasab, Mehran; Moghadamtousi, Soheil Zorofchian; Hajrezaei, Maryam; Zahedifard, Maryam; Razavi, Mahboubeh; Safi, Sher Zaman; Mohan, Syam; Khalifa, Shaden A. M.; El‐Seedi, Hesham R.; Abdulla, Mahmood Amin; Ali, Hapipah Mohd; Noordin, Mohamed Ibrahim

doi:10.1159/000430273

Cited by 16 publications

(12 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Cyclin-dependent kinase p21 is tumor suppressor, which promotes cell cycle arrest, blocks cell division, and down-regulation of p21 often occurs in breast cancer [31]. Recent studies have demonstrated that p21 involved in anti-tumor progression in breast cancer, and anti-tumor drug increased p21 expression which led to breast cancer cell apoptosis [32,33]. p73 and p21 can promote anti-proliferation activity and induce apoptosis by p53-independent mechanisms [34,35].…”

Section: Discussionmentioning

confidence: 99%

Antiproliferative Effect of Androgen Receptor Inhibition in Mesenchymal Stem-Like Triple-Negative Breast Cancer

Zhu

Song

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Androgen receptor (AR), a steroid hormone receptor, has recently emerged as prognostic and treatment-predictive marker in breast cancer. Previous studies have shown that AR is widely expressed in up to one-third of triple-negative breast cancer (TNBC). However, the role of AR in TNBC is still not fully understood, especially in mesenchymal stem-like (MSL) TNBC cells. Methods: MSL TNBC MDA-MB-231 and Hs578T breast cancer cells were exposed to various concentration of agonist 5-α-dihydrotestosterone (DHT) or nonsteroidal antagonist bicalutamide or untreated. The effects of AR on cell viability and apoptosis were determined by MTT assay, cell counting, flow cytometry analysis and protein expression of p53, p73, p21 and Cyclin D1 were analyzed by western blotting. The bindings of AR to p73 and p21 promoter were detected by ChIP assay. MDA-MB-231 cells were transplanted into nude mice and the tumor growth curves were determined and expression of AR, p73 and p21 were detected by Immunohistochemistry (IHC) staining after treatment of DHT or bicalutamide. Results: We demonstrate that AR agonist DHT induces MSL TNBC breast cancer cells proliferation and inhibits apoptosis in vitro. Similarly, activated AR significantly increases viability of MDA-MB-231 xenografts in vivo. On the contrary, AR antagonist, bicalutamide, causes apoptosis and exerts inhibitory effects on the growth of breast cancer. Moreover, DHT-dependent activation of AR involves regulation in the cell cycle related genes, including p73, p21 and Cyclin D1. Further investigations indicate the modulation of AR on p73 and p21 mediated by direct binding of AR to their promoters, and DHT could make these binding more effectively. Conclusions: Our study demonstrates the tumorigenesis role of AR and the inhibitory effect of bicalutamide in AR-positive MSL TNBC both in vitro and in vivo, suggesting that AR inhibition could be a potential therapeutic approach for AR-positive TNBC patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Antiproliferative Effect of Androgen Receptor Inhibition in Mesenchymal Stem-Like Triple-Negative Breast Cancer

Zhu

Song

et al. 2016

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…Interruption or malformation of the cell plasma membrane which is a common property of cancer cells causes the cell construction losing and break of their life cycle [ 39 ]. Phosphatidylserine (PS) translocation from the inner side of the plasma membrane to the outer side of the plasma membrane is a typical marker of early apoptosis.…”

Section: Resultsmentioning

confidence: 99%

“…Fig 2E also shows that the cell population in S phase decreased from 26.81% to 6.77%, while the percentage of the population in G2/M phase decreased from 20.01% to 3.41%. The cyclin-dependent kinases (CDKs) have a critical role in cell cycle control through their interaction with cyclins and Cdk inhibitors (CKIs) [ 39 ]. The irregular growth of cancer cells is associated with the abnormal activity of CKIs.…”

Section: Resultsmentioning

confidence: 99%

Monobenzyltin Complex C1 Induces Apoptosis in MCF-7 Breast Cancer Cells through the Intrinsic Signaling Pathway and through the Targeting of MCF-7-Derived Breast Cancer Stem Cells via the Wnt/β-Catenin Signaling Pathway

et al. 2016

Self Cite

View full text Add to dashboard Cite

Monobenzyltin Schiff base complex, [N-(3,5-dichloro-2-oxidobenzylidene)-4-chlorobenzyhydrazidato](o-methylbenzyl)aquatin(IV) chloride, C1, is an organotin non-platinum metal-based agent. The present study was conducted to investigate its effects on MCF-7 cells with respect to the induction of apoptosis and its inhibitory effect against MCF-7 breast cancer stem cells. As determined in a previous study, compound C1 revealed strong antiproliferative activity on MCF-7 cells with an IC50 value of 2.5 μg/mL. Annexin V/propidium iodide staining coupled with flow cytometry indicated the induction of apoptosis in treated cells. Compound C1 induced apoptosis in MCF-7 cells and was mediated through the intrinsic pathway with a reduction in mitochondrial membrane potential and mitochondrial cytochrome c release to cytosol. Complex C1 activated caspase 9 as a result of cytochrome c release. Subsequently, western blot and real time PCR revealed a significant increase in Bax and Bad expression and a significant decrease in the expression levels of Bcl2 and HSP70. Furthermore, a flow cytometric analysis showed that treatment with compound C1 caused a significant arrest of MCF-7 cells in G0/G1 phase. The inhibitory analysis of compound C1 against derived MCF-7 stem cells showed a significant reduction in the aldehyde dehydrogenase-positive cell population and a significant reduction in the population of MCF-7 cancer stem cells in primary, secondary, and tertiary mammospheres. Moreover, treatment with C1 down-regulated the Wnt/β-catenin self-renewal pathway. These findings indicate that complex C1 is a suppressive agent of MCF-7 cells that functions through the induction of apoptosis, cell cycle arrest, and the targeting of MCF-7-derived cancer stem cells. This work may lead to a better treatment strategy for the reduction of breast cancer recurrence.

show abstract

“…Breast cancer is the most common malignancy among women presenting an emerging major health problem around the world and the number of cases of has increased dramatically in Asia over the past few decades [1][2][3][4] . The development drug resistance in breast cancer is a growing challenge in the field of cancer therapy.…”

Section: Research Papermentioning

confidence: 99%

Antitumor Studies of Earthworm Fibrinolytic Enzyme Component A from Eisenia foetida on Breast Cancer Cell Line MCF-7

Liu¹,

Chen²,

Pan³

et al. 2017

pharmaceutical-sciences

View full text Add to dashboard Cite

Liu, et al.: Antitumor Studies of Earthworm Fibrinolytic Enzyme Component A on MCF-7Earthworm fibrinolytic enzyme from Chinese earthworm Eisenia foetida was isolated to investigate its antitumor activity in breast cancer cells. The protein isolated was characterised as earthworm fibrinolytic enzyme using the fibrin plate method. The molecular weight of earthworm fibrinolytic enzyme component was determined to be 25 kDa by sodium dodecyl sulfate polyacrylamide gel electrophoresis assay using a standard protein ladder. Earthworm fibrinolytic enzyme can markedly inhibit the growth and migration of MCF-7 cells in a dose and time-dependent manner. In addition, MCF-7 cells treated with earthworm fibrinolytic enzyme (40 μg/ml) began to undergo apoptosis after 24 h. Expression of focal adhesion kinase and CD44v6 measured using reverse transcription polymerase chain reaction and Western blot was down-regulated in a concentration-dependent manner (20-80 μg/ml), resulting in the suppression of MCF-7 cells adhesion. The obtained earthworm fibrinolytic enzyme displayed an antitumor effect on MCF-7 cells in vitro, revealing the therapeutic potential of E. foetida.

show abstract

The Chemopreventive Effect of Tanacetum Polycephalum Against LA7-Induced Breast Cancer in Rats and the Apoptotic Effect of a Cytotoxic Sesquiterpene Lactone in MCF7 Cells: A Bioassay-Guided Approach

Cited by 16 publications

References 51 publications

Antiproliferative Effect of Androgen Receptor Inhibition in Mesenchymal Stem-Like Triple-Negative Breast Cancer

Antiproliferative Effect of Androgen Receptor Inhibition in Mesenchymal Stem-Like Triple-Negative Breast Cancer

Monobenzyltin Complex C1 Induces Apoptosis in MCF-7 Breast Cancer Cells through the Intrinsic Signaling Pathway and through the Targeting of MCF-7-Derived Breast Cancer Stem Cells via the Wnt/β-Catenin Signaling Pathway

Antitumor Studies of Earthworm Fibrinolytic Enzyme Component A from Eisenia foetida on Breast Cancer Cell Line MCF-7

Contact Info

Product

Resources

About