Phthalates induce proliferation and invasiveness of estrogen receptor‐negative breast cancer through the AhR/HDAC6/c‐Myc signaling pathway

@article{Hsieh2012PhthalatesIP,
  title={Phthalates induce proliferation and invasiveness of estrogen receptor‐negative breast cancer through the AhR/HDAC6/c‐Myc signaling pathway},
  author={Tsung-Hua Hsieh and Cheng-Fang Tsai and Chia-Yi Hsu and Po-Lin Kuo and Jau-nan Lee and Chee-Yin Chai and Shao-Chun Wang and Eing-Mei Tsai},
  journal={The FASEB Journal},
  year={2012},
  volume={26},
  pages={778 - 787}
}
The environmentally present group of chemical phthalates, or phthalate esters, has been recognized as a rising threat to public health, including cancer. While most studies have addressed the estrogenic effects of phthalates in malignancies of the breast and the prostate, little is known about their role in the etiology of hormone‐independent cancer. Here we show that treatments with the phthalates n‐butyl benzyl phthalate (BBP) and dibutyl phthalate (DBP) at 1 μM induced proliferation (BBP, 3… 
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Butyl benzyl phthalate promotes prostate cancer cell proliferation through miR-34a downregulation.
n-Butyl Benzyl Phthalate Promotes Breast Cancer Progression by Inducing Expression of Lymphoid Enhancer Factor 1
TLDR
The altered expression of this gene consistently differentiated tumors expressing genes involved in proliferation, epithelial-mesenchymal transition, and angiogenesis, contributing to the understanding of the molecular impact of the environmental hormone BBP and suggest possible strategies for preventing and treating human breast cancer.
Phthalates promote prostate cancer cell proliferation through activation of ERK5 and p38.
Exposure to parabens at the concentration of maximal proliferative response increases migratory and invasive activity of human breast cancer cells in vitro
TLDR
This is the first report that in vitro, parabens can influence not only proliferation but also migratory and invasive properties of human breast cancer cells.
miR-19 targeting of PTEN mediates butyl benzyl phthalate-induced proliferation in both ER(+) and ER(-) breast cancer cells.
Phthalate exposure promotes chemotherapeutic drug resistance in colon cancer cells
TLDR
Results suggest phthalate exposure enhances colon cancer cell metastasis and chemotherapeutic drug resistance by increasing cancer cell stemness, and that P-glycoprotein inhibitors might improve outcomes for advanced or drug-resistant colon cancer patients.
Phthalates stimulate the epithelial to mesenchymal transition through an HDAC6-dependent mechanism in human breast epithelial stem cells.
TLDR
Molecular mechanism studies revealed that histone deacetylase 6 (HDAC6) is required for phthalate-induced cell migration and invasion during EMT in vitro and metastasis into the lungs of nude mice.
Mechanism of phthalate esters in the progression and development of breast cancer.
TLDR
The phthalates are able to mimic estrogen, to prompt proliferation, metastasis and drug resistance in breast cancer cells, and the data for its dosage exposure to induce ill-effects remains largely inconsistent.
TCDD-induced antagonism of MEHP-mediated migration and invasion partly involves aryl hydrocarbon receptor in MCF7 breast cancer cells.
Didymin reverses phthalate ester-associated breast cancer aggravation in the breast cancer tumor microenvironment.
TLDR
It is suggested that didymin, a dietary flavonoid glycoside present in citrus fruits, was capable of preventing phthalate ester-associated cancer aggravation.
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References

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