Estrogen receptor beta decreases survival of p53-defective cancer cells after DNA damage by impairing G2/M checkpoint signaling

@article{Thomas2010EstrogenRB,
  title={Estrogen receptor beta decreases survival of p53-defective cancer cells after DNA damage by impairing G2/M checkpoint signaling},
  author={Christoforos Thomas and Anders M. Strom and Karolina Lindberg and Jan-{\AA}ke Gustafsson},
  journal={Breast Cancer Research and Treatment},
  year={2010},
  volume={127},
  pages={417-427}
}
Estrogen receptor beta (ERβ) inhibits proliferation in different cellular systems by regulating components of the cell cycle machinery. Eukaryotic cells respond to DNA damage by arresting in G1, S, or G2 phases of the cell cycle to initiate DNA repair. Most tumor cells due to disruptions in the p53-dependent G1 pathway are dependent on S-phase and G2/M checkpoints to maintain genomic integrity in response to DNA damage. We report that induction of ERβ expression causes abrogation of the S-phase… 
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51 Citations
Background Citations
21
Methods Citations
3
Results Citations
7

51 Citations

ERβ Sensitizes NSCLC to Chemotherapy by Regulating DNA Damage Response

Upregulation of ERβ1 increases the sensitivity of NSCLC cells to treatment with doxorubicin and etoposide and supports the potential predictive and therapeutic value of the receptor in clinical management of the disease.

Estrogen receptor beta enhances chemotherapy response of GBM cells by down regulating DNA damage response pathways

Mechanical studies showed that ERβ plays an important role in homologous recombination (HR) mediated repair and ERβ reduced expression and activation of ATM upon DNA damage and the evidence is provided that ER β is required for optimal chemotherapy induced DNA damage response and apoptosis in GBM cells.

Estrogen Signaling and the DNA Damage Response in Hormone Dependent Breast Cancers

The hypothesis that estrogen receptor signaling converges to suppress effective DNA repair and apoptosis in favor of proliferation is put forward in hormone-dependent breast cancer as it will affect processing of estrogen-induced DNA damage, as well as other genotoxic insults.

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The results suggest a collaboration of ERβ and p53 tumor suppressor activity in breast cancer cells that indicates the importance of ligand-regulated ERβ as a tool to target p53 activity and improve the clinical management of resistant disease.

The p53-estrogen receptor loop in cancer.

This review will summarize the current body of knowledge on p53, ERα and ERβ in cancer and discuss the relationship between p53 and ERs at both the molecular and clinical levels.

Estrogen receptor β isoform 5 confers sensitivity of breast cancer cell lines to chemotherapeutic agent-induced apoptosis through interaction with Bcl2L12.

In conclusion, ERβ5 interacts with Bcl2L12 and functions in a novel estrogen-independent molecular pathway that promotes chemotherapeutic Agent-Induced in vitro apoptosis of BCa cell lines.

Somatic loss of estrogen receptor beta and p53 synergize to induce breast tumorigenesis

Somatic loss of ERβ significantly accelerated formation of p53-deficient mammary tumors and resulted in the development of less differentiated carcinomas with stronger spindle cell morphology and decreased expression of luminal epithelial markers.

ERβ decreases breast cancer cell survival by regulating the IRE1/XBP-1 pathway

Upregulation of wild-type ERβ (ERβ1) or treatment with ERβ agonists enhanced apoptosis in breast cancer cells in the presence of pharmacological inducers of EnR stress, suggesting that the ability of ERβ1 to target the UPR may offer alternative treatment strategies for breast cancer.

ERβ Regulates NSCLC Phenotypes by Controlling Oncogenic RAS Signaling

It is demonstrated that ERβ1 decreases the survival of NSCLC cells by regulating oncogenic RAS signaling and downregulation of EGFR and inactivation of RAS and the downstream components ERK1/2 were found to be involved in the ER β1-induced apoptosis.

Roles of Estrogens in Prostate Cancer Development via the Modulation of DNA-Repair System

The function of DNA repair molecules is reviewed at a viewpoint of prostate carcinogenesis and of lifestyle related DNA damages, providing an understanding on the molecular mechanisms by which estrogen may employ their action on the regulation of prostate cancer.
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