Aryl Hydrocarbon Receptor Mediates Sensitivity of MCF-7 Breast Cancer Cells to Antitumor Agent 2-(4-Amino-3-methylphenyl) Benzothiazole

2002 ◽  
Vol 61 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Andrea I. Loaiza-Pérez ◽  
Valentina Trapani ◽  
Curtis Hose ◽  
Sheo S. Singh ◽  
Jane B. Trepel ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Antitumor Agent ◽  
Aryl Hydrocarbon ◽  
Mcf 7

scholarly journals The Role of Aryl Hydrocarbon Receptor and Crosstalk with Estrogen Receptor in Response of Breast Cancer Cells to the Novel Antitumor Agents Benzothiazoles and Aminoflavone

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Mariana A. Callero ◽  
Andrea I. Loaiza-Pérez
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Antitumor Agents ◽  
Breast Cancers ◽  
Nude Mouse Model ◽  
Aryl Hydrocarbon ◽  
Mcf 7

Many estrogen-receptor- (ER-) expressing breast cancers become refractory to ER-based therapies. New antitumor drugs like aminoflavone (AF) and benzothiazoles (Bzs) have been developed and have exquisite antitumor activity in ER+MCF-7 and T47D cells and in a MCF-7 nude mouse model. ER(−) breast cancer cells like MDA-MB-231 are less susceptible. We previously found in MCF-7 cells that these drugs activate the aryl hydrocarbon receptor (AhR) via translocation to the nucleus, induction of AhR-specific DNA binding activity, and expression of CYP1A1, whose transcription is controlled by the AhR-ARNT transcription factor. CYP1A1 metabolizes AF and Bz to a species which directly or after further metabolism damages DNA. In contrast an AhR-deficient variant of MCF-7 or cells with predominantly nuclear AhR expression, such as MDA-MB 231, are resistant. Thus, these drugs, unlike other neoplastic agents, require AhR-mediated signaling to cause DNA damage. This is a new treatment strategy for breast cancers with intact AhR signaling.

scholarly journals Berberine Activates Aryl Hydrocarbon Receptor but Suppresses CYP1A1 Induction through miR-21-3p Stimulation in MCF-7 Breast Cancer Cells

Molecules ◽  
2017 ◽  
Vol 22 (11) ◽  
pp. 1847 ◽  
Author(s):  
Sheng-Nan Lo ◽  
Chun-Wei Wang ◽  
Yueh-Shieh Chen ◽  
Chiung-Chiao Huang ◽  
Tian-Shung Wu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Aryl Hydrocarbon ◽  
Cyp1a1 Induction ◽  
Mcf 7

Conditional expression of a constitutively active aryl hydrocarbon receptor in MCF-7 human breast cancer cells

2002 ◽  
Vol 402 (2) ◽  
pp. 172-179 ◽  
Author(s):  
Christoph Köhle ◽  
Ingo Hassepass ◽  
Barbara S Bock-Hennig ◽  
Karl Walter Bock ◽  
Lorenz Poellinger ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Aryl Hydrocarbon ◽  
Conditional Expression ◽  
Mcf 7

scholarly journals Expression of the aryl hydrocarbon receptor is not required for the proliferation, migration, invasion, or estrogen-dependent tumorigenesis of MCF-7 breast cancer cells

2012 ◽  
Vol 52 (7) ◽  
pp. 544-554 ◽  
Author(s):  
Barbara C. Spink ◽  
James A. Bennett ◽  
Nicole Lostritto ◽  
Jacquelyn R. Cole ◽  
David C. Spink
Keyword(s):  
Breast Cancer ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Aryl Hydrocarbon ◽  
Mcf 7

Aryl hydrocarbon receptor agonists directly activate estrogen receptor α in MCF-7 breast cancer cells

2006 ◽  
Vol 387 (9) ◽  
Author(s):  
Shengxi Liu ◽  
Maen Abdelrahim ◽  
Shaheen Khan ◽  
Eric Ariazi ◽  
V. Craig Jordan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Estrogen Receptor Α ◽  
Receptor Agonists ◽  
Aryl Hydrocarbon ◽  
Mcf 7

scholarly journals Emodin Inhibits the Proliferation of MCF-7 Human Breast Cancer Cells Through Activation of Aryl Hydrocarbon Receptor (AhR)

2021 ◽  
Vol 11 ◽  
Author(s):  
Ning Zhang ◽  
Jiawen Wang ◽  
Aimin Sheng ◽  
Shuo Huang ◽  
Yanyan Tang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Dependent Manner ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Aryl Hydrocarbon ◽  
Mcf 7

Natural products have proved to be a promising source for the development of potential anticancer drugs. Emodin, a natural compound from Rheum palmatum, is used to treat several types of cancers, including lung, liver, and pancreatic. However, there are few reports regarding its use in the treatment of breast cancer. Thus, the therapeutic effect and mechanism of emodin on MCF-7 human breast cancer cells were investigated in this study. Morphological observations and cell viability were evaluated to determine the anti-proliferation activity of emodin. Network pharmacology and molecular docking were performed to screen the potential targets. Western blot analysis was used to explore a potential antitumor mechanism. The results showed that emodin (50–100 μmol/L) could significantly inhibit the proliferation of MCF-7 cells in a time and dose-dependent manner. Furthermore, virtual screening studies indicated that emodin was a potent aryl hydrocarbon receptor (AhR) agonist in chemotherapy for breast cancer. Finally, when MCF-7 cells were treated with emodin (100 μmol/L) for 24 h, the AhR and cytochrome P450 1A1 (CYP1A1) protein expression levels were significantly upregulated compared with the control group. Our study indicated that emodin exhibited promising antitumor activity in MCF-7 cells, likely through activation of the AhR-CYP1A1 signaling pathway. These findings lay a foundation for the application of emodin in breast cancer treatment.

scholarly journals microRNA-548m suppresses cell migration and invasion by targeting aryl hydrocarbon receptor in breast cancer cells

2020 ◽  
Author(s):  
WM Farhan Syafiq B WM Nor ◽  
Ivy Chung ◽  
Nur Akmarina B M Said
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Aryl Hydrocarbon Receptor ◽  
Cancer Cells ◽  
Cell Lines ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Cell Migration And Invasion ◽  
Aryl Hydrocarbon ◽  
Mcf 7

Breast cancer is the most commonly diagnosed cancer among women and one of the leading causes of cancer mortality worldwide, in which the most severe form happens when it metastasizes to other regions of the body. Metastasis is responsible for most treatment failures in advanced breast cancer. Epithelial-mesenchymal transition (EMT) plays a significant role in promoting metastatic processes in breast cancer. MicroRNAs (miRNAs) are highly conserved endogenous short non-coding RNAs that play a role in regulating a broad range of biological processes, including cancer initiation and development, by functioning as tumor promoters or tumor suppressors. Expression of miR-548m has been found in various types of cancers, but the biological function and molecular mechanisms of miR-548m in cancers have not been fully studied. Here, we demonstrated the role of miR-548m in modulating EMT in the breast cancer cell lines MDA-MB-231 and MCF-7. Expression data for primary breast cancer obtained from NCBI GEO datasets showed that miR-548m expression was downregulated in breast cancer patients compared with healthy group. We hypothesize that miR-548m acts as a tumor suppressor in breast cancer. Overexpression of miR-548m in both cell lines increased E-cadherin expression and decreased the EMT-associated transcription factors SNAI1, SNAI2, ZEB1 and ZEB2, as well as MMP9 expression. Consequently, migration and invasion capabilities of both MDA-MB-231 and MCF-7 cells were significantly inhibited in miR-548m-overexpressing cells. Analysis of 1059 putative target genes of miR-548m revealed common pathways involving both tight junction and the mTOR signaling pathway, which has potential impacts on cell migration and invasion. Furthermore, this study identified aryl hydrocarbon receptor (AHR) as a direct target of miR-548m in breast cancer cells. Taken together, our findings suggest a novel function of miR-548m in reversing the EMT of breast cancer by reducing their migratory and invasive potentials, at least in part via targeting AHR expression.

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