Estradiol receptors in breast cancer cells: Associated co-factors as targets for new therapeutic approaches

Steroids ◽  
2012 ◽  
Vol 77 (12) ◽  
pp. 1249-1261 ◽  
Author(s):  
Jack-Michel Renoir
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Therapeutic Approaches ◽  
New Therapeutic Approaches ◽  
Estradiol Receptors

scholarly journals VGLL1-directed TEAD activation drives endocrine therapy resistance in estrogen receptor positive breast cancer

2020 ◽  
Author(s):  
Carolina Gemma ◽  
Anup K Singh ◽  
Antonino Belfiore ◽  
Chun-Fui Lai ◽  
Manikandan Periyasamy ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Standard Of Care ◽  
Therapy Resistance ◽  
Breast Cancer Patients ◽  
New Therapeutic Approaches ◽  
Positive Breast Cancer ◽  
Resistant Cells

AbstractEndocrine therapies are standard-of-care treatments for estrogen receptor (ER) positive breast cancer. However, patients with ER+ breast cancer develop resistance to these therapies and most relapsed patients die with endocrine-resistant metastatic disease. Here we show that resistance to the ER degrader, fulvestrant, is accompanied by epigenetic activation of the transcriptional co-activator VGLL1. Rewiring of the epigenome in therapy resistant cells also results in increased binding of the transcription factor TEAD4. Through interaction with TEAD4, VGLL1 induces the expression of genes implicated in cell proliferation in the resistant cells. We demonstrate that VGLL1 is necessary for the growth of fulvestrant-resistant breast cancer cells. Pharmacological disruption of VGLL1/TEAD4 interaction blocked growth of fulvestrant-resistant cells, accompanied by inhibition of VGLL1/TEAD transcriptional programmes. Furthermore, we identify EGFR as an important downstream VGLL1 target, whereby VGLL1-directed EGFR upregulation sensitises fulvestrant-resistant breast cancer cells to EGFR inhibitors. Taken together, our findings identify VGLL1 as a key transcriptional driver in endocrine-resistant breast cancer and identify new therapeutic approaches for advanced breast cancer patients.

scholarly journals ANKRD22 enhances breast cancer cell malignancy by activating the Wnt/β-catenin pathway via modulating NuSAP1 expression

2020 ◽  
Author(s):  
Yange Wu ◽  
Hongxia Liu ◽  
Yufeng Gong ◽  
Bo Zhang ◽  
Wenxiu Chen
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Normal Breast ◽  
Mesenchymal Transition ◽  
New Therapeutic Approaches ◽  
Cell Malignancy

Breast cancer is one of the most prevalent malignancies in women worldwide. Although great progress has been achieved in the diagnosis and treatment of breast cancer, the prognosis of patients with breast cancer is still poor due to distal recurrence and metastasis after surgery. This study demonstrated that the expression level of ankyrin repeat domain 22 (ANKRD22) in human breast cancer tissues was significantly higher than that in normal breast tissues. ANKRD22 knockdown inhibited the proliferation, invasion, and epithelial-mesenchymal transition (EMT) of breast cancer cells. Further research indicated that ANKRD22 regulated the expression of nucleolar and spindle-associated protein 1 (NuSAP1) and then the activation of Wnt/β-catenin signaling pathway. Moreover, overexpression of NuSAP1 reversed the inhibitory effects of ANKRD22 knockdown on the proliferation, invasion, and EMT of breast cancer cells. In summary, this study demonstrated that ANKRD22 enhanced breast cancer cell malignancy by activating the Wnt/β-catenin pathway via modulating NuSAP1 expression, which might shed light on new therapeutic approaches for breast cancer.

The proliferation of breast cancer cells are inhibited by the human intrabody targeting cyclinD1

2010 ◽  
Vol 34 (8) ◽  
pp. S49-S49
Author(s):  
Lei Wang ◽  
Xun Zhou ◽  
Lihong Zhou ◽  
Yong Chen ◽  
Xun Zhu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells

Asperjinone, a norneolignan, and terrein, a suppressor of ABCG2-expressing breast cancer cells, from Aspergillus terreus

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
WY Liao ◽  
CN Shen ◽  
LH Lin ◽  
YL Yang ◽  
HY Han ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Aspergillus Terreus
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