Multiple omics analysis of the protective effects of SFN on estrogen-dependent breast cancer cells

2020 ◽  
Vol 47 (5) ◽  
pp. 3331-3346
Author(s):  
Hui Huang ◽  
Shuyuan Cao ◽  
Zhan Zhang ◽  
Lei Li ◽  
Feng Chen ◽  
...  
2019 ◽  
Vol 17 (2) ◽  
pp. 132-140 ◽  
Author(s):  
Carlos R. Oliveira ◽  
Daniel G. Spindola ◽  
Daniel M. Garcia ◽  
Adolfo Erustes ◽  
Alexandre Bechara ◽  
...  

Cancers ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1011 ◽  
Author(s):  
Javier Menéndez-Menéndez ◽  
Francisco Hermida-Prado ◽  
Rocío Granda-Díaz ◽  
Alicia González ◽  
Juana María García-Pedrero ◽  
...  

Melatonin mitigates cancer initiation, progression and metastasis through inhibition of both the synthesis of estrogens and the transcriptional activity of the estradiol-ER (Estrogen receptor) complex in the estrogen-dependent breast cancer cell line MCF-7. Moreover, melatonin improves the sensitivity of MCF-7 to chemotherapeutic agents and protects against their side effects. It has been described that melatonin potentiates the anti-proliferative effects of doxorubicin; however, the molecular changes involving gene expression and the activation/inhibition of intracellular signaling pathways remain largely unknown. Here we found that melatonin enhanced the anti-proliferative effect of doxorubicin in MCF-7 but not in MDA-MB-231 cells. Strikingly, doxorubicin treatment induced cell migration and invasion, and melatonin effectively counteracted these effects in MCF-7 but not in estrogen-independent MDA-MB-231 cells. Importantly, we describe for the first time the ability of melatonin to downregulate TWIST1 (Twist-related protein 1) in estrogen-dependent but not in estrogen-independent breast cancer cells. Combined with doxorubicin, melatonin inhibited the activation of p70S6K and modulated the expression of breast cancer, angiogenesis and clock genes. Moreover, melatonin regulates the levels of TWIST1-related microRNAs, such as miR-10a, miR-10b and miR-34a. Since TWIST1 plays a pivotal role in the epithelial to mesenchymal transition, acquisition of metastatic phenotype and angiogenesis, our results suggest that inhibition of TWIST1 by melatonin might be a crucial mechanism of overcoming resistance and improving the oncostatic potential of doxorubicin in estrogen-dependent breast cancer cells.


Medicines ◽  
2017 ◽  
Vol 4 (3) ◽  
pp. 56 ◽  
Author(s):  
Meran Keshawa Ediriweera ◽  
Kamani Hemamala Tennekoon ◽  
Sameera Ranganath Samarakoon ◽  
Ira Thabrew ◽  
E. Dilip de Silva

2020 ◽  
Vol 29 ◽  
pp. 096368972092027
Author(s):  
Zhiyan Shan ◽  
Li Liu ◽  
Jingling Shen ◽  
Haiyue Hao ◽  
Honghong Zhang ◽  
...  

Purpose: Death domain–associated protein (DAXX) is a multifunctional nuclear protein involved in apoptosis, transcription, deoxyribonucleic acid damage response, and tumorigenesis. However, the role of DAXX in breast cancer development and progression remains elusive. In this study, we examined the expression patterns and function of DAXX in human breast cancer samples and cell lines. Methods: Immunohistochemistry was used to analyze the expression and localization patterns of DAXX. Additionally, we investigated whether DAXX played an intrinsic role in the cellular response to damage induced by ultraviolet (UV) irradiation in MDA-MB-231 breast cancer cells (isolated at M D Anderson from a pleural effusion of a patient with invasive ductal carcinoma). Results: Our results showed that nucleus size, chromatin organization, and DAXX localization were altered in breast cancer tissues compared with those in control tissues. Compared with cytoplasmic and nuclear expression in benign breast tissues, DAXX was colocalized with promyelocytic leukemia in nuclei with a granular distribution. Endogenous DAXX messenger ribonucleic acid levels were upregulated upon UV radiation in MDA-MB-231 cells. DAXX-deficient cells tended to be more sensitive to irradiation than control cells. Conversely, DAXX-overexpressing cells exhibited reduced phosphorylated histone H2AX (γ-H2AX) accumulation, increased cell survival, and resistance to UV-induced damage. The protective effects of DAXX may be related to the activation of the ataxia telangiectasia mutated (ATM)-checkpoint kinase 2 (ATM-CHK2)-cell division cycle 25c (CDC25c) signaling pathways in Gap2/Mitosis (G2/M) checkpoint and ultimately cell cycle arrest at G2/M phase. Conclusions: Taken together, these results suggested that DAXX may be an essential component in breast cancer initiation, malignant progression, and radioresistance.


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

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