scholarly journals Antioxidants for the Treatment of Breast Cancer: Are We There Yet?

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 205
Author(s):  
Carmen Griñan-Lison ◽  
Jose L. Blaya-Cánovas ◽  
Araceli López-Tejada ◽  
Marta Ávalos-Moreno ◽  
Alba Navarro-Ocón ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Cancer Progression ◽  
Redox Homeostasis ◽  
Breast Carcinogenesis ◽  
Breast Cancer Patients ◽  
Chemopreventive Agents ◽  
Low Degree ◽  
Potential Use

Breast cancer is the most frequent cancer and the leading cause of cancer death in women. Oxidative stress and the generation of reactive oxygen species (ROS) have been related to cancer progression. Compared to their normal counterparts, tumor cells show higher ROS levels and tight regulation of REDOX homeostasis to maintain a low degree of oxidative stress. Traditionally antioxidants have been extensively investigated to counteract breast carcinogenesis and tumor progression as chemopreventive agents; however, there is growing evidence indicating their potential as adjuvants for the treatment of breast cancer. Aimed to elucidate whether antioxidants could be a reality in the management of breast cancer patients, this review focuses on the latest investigations regarding the ambivalent role of antioxidants in the development of breast cancer, with special attention to the results derived from clinical trials, as well as their potential use as plausible agents in combination therapy and their power to ameliorate the side effects attributed to standard therapeutics. Data retrieved herein suggest that antioxidants play an important role in breast cancer prevention and the improvement of therapeutic efficacy; nevertheless, appropriate patient stratification based on “redoxidomics” or tumor subtype is mandatory in order to define the dosage for future standardized and personalized treatments of patients.

scholarly journals Mechanisms of Metastasis and Cell Mobility – The Role of Metabolism

2019 ◽  
Vol 79 (02) ◽  
pp. 184-188 ◽  
Author(s):  
Carsten Gründker ◽  
Matthias Läsche ◽  
Johanna Hellinger ◽  
Günter Emons
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Early Stage ◽  
Breast Cancer Patients ◽  
Metastatic Cascade ◽  
Cell Mobility ◽  
Tumour Metastasis ◽  
Multi Stage ◽  
Mesenchymal Transformation

AbstractTumour metastasis is responsible for more than 90% of tumour-associated mortality. About one third of breast cancer patients in the early stage develop metastases. The transformation in tumour development referred to as the “metastatic cascade” or “metastatic cycle” is a complex and multi-stage event. While it is generally recognised that epithelial-mesenchymal transformation (EMT) plays a crucial role in cancer progression and metastasis, the metabolic events in this process have received little attention to date. We would therefore like to provide a brief overview here of the influence of the metabolism on the progression and metastasis of tumours.

scholarly journals Model-based in silico analysis of the PI3K/Akt pathway: the elucidation of cross-talk between diabetes and breast cancer

PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e5917 ◽  
Author(s):  
Sammia Rehman ◽  
Ayesha Obaid ◽  
Anam Naz ◽  
Amjad Ali ◽  
Shahzina Kanwal ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Insulin Signaling ◽  
In Silico ◽  
In Silico Analysis ◽  
Positive Association ◽  
Pi3k Pathway ◽  
Diabetic Patients ◽  
Breast Cancer Patients

Background A positive association between diabetes and breast cancer has been identified by various epidemiological and clinical studies. However, the possible molecular interactions between the two heterogeneous diseases have not been fully determined yet. There are several underlying mechanisms which may increase the risk of breast cancer in diabetic patients. Introduction In this study, we focused on the role of O-GlcNAc transferase (OGT) enzyme in the regulation of phosphatidylinositol-3 kinase (PI3K) pathway through activation/deactivation of Akt protein. The efficiency of insulin signaling in adipocytes is reduced as a result of OGT overexpression which further attenuates Akt signaling; as a result, the efficiency of insulin signaling is reduced by downregulation of insulin-responsive genes. On the other hand, increased expression of OGT results in Akt activation in breast cancer cells, leading to enhanced cell proliferation and inhibition of the apoptosis. However, the interplay amongst these signaling pathways is still under investigation. Methods In this study, we used Petri nets (PNs) to model and investigate the role of PI3K and OGT pathways, acting as key players in crosstalk between diabetes and breast cancer, resulting in progression of these chronic diseases. Moreover, in silico perturbation experiments were applied on the model to analyze the effects of anti-cancer agents (shRNA and BZX) and anti-diabetic drug (Metformin) on the system. Results Our PN model reflects the alterations in protein expression and behavior and the correlation between breast cancer and diabetes. The analysis proposed two combination therapies to combat breast cancer progression in diabetic patients including combination of OGTmRNA silencing and OGT inhibitor (BZX) as first combination and BZX and Metformin as the second. Conclusion The PN model verified that alterations in O-GlcNAc signaling affect both insulin resistance and breast cancer. Moreover, the combination therapy for breast cancer patients consisting of anti-diabetic drugs such as Metformin along with OGT inhibitors, for example BZX, can produce better treatment regimens.

scholarly journals Production of Reactive Oxygen Species, Unbalanced by Endogenous Antioxidant Capture Mechanisms Monitored in Surgically Treated Breast Cancer

2020 ◽  
Vol 71 (4) ◽  
pp. 456-471
Author(s):  
Alina Oana Rusu-Moldovan ◽  
Maria Iuliana Gruia ◽  
Camelia-Manuela Mirza ◽  
Dan Mihu
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Redox Balance ◽  
Mitotic Rate ◽  
Breast Cancer Patients ◽  
Treated Breast ◽  
Endogenous Antioxidant ◽  
Therapy Strategies ◽  
Treated Breast Cancer

Oxidative stress is defined as an imbalance between the production of oxygen reactive species (ROS) and their endogenous capacity of capturing them. Oxidative stress activates multiple effects generated by the non-specific growth of the ROS and by the decrease of antioxidant concentrations and neutralization mechanisms. The most accurate understanding of the mechanisms underlying oxidative stress and the deepening of its implications in different cancers has become very important in recent decades. Cancer cells are usually subjected to high levels of ROS, which continually activates the malignant phenotype by stimulating cell proliferation � by increasing the mitotic rate, angiogenesis, invasiveness and metastasis rates. The role of the ROS in the etiology and progression of breast cancer is in continuous processing. However, less attention has been paid to the development of redox-targeted breast cancer therapy strategies. Excess ROS production is detrimental for the survival and proliferation of neoplastic cells, through the oxidative-destructive mechanisms of biomolecules essential for life. This study departs from the hypothesis that the tumor is an inductive factor of oxidative stress, and an antioxidant treatment prior to surgery may influence the response to surgical treatment in breast cancer patients. This response is highlighted by determining certain essential compounds of the redox balance, after initiating the antioxidant therapy. Moreover, we have tried to assess the possible biochemical changes given by age, tumor size and asymmetry/laterality of the neoplasm in the investigated patients, and to determine the prognostic or predictive factors of these changes.

Increased YAP1 expression is significantly associated with breast cancer progression, metastasis and poor survival

2021 ◽  
Author(s):  
Javeria Qadir ◽  
Syeda Kiran Riaz ◽  
Kiran Taj ◽  
Natasha Sattar ◽  
Namood-e Sahar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Patients ◽  
Cancer Progression ◽  
Hippo Pathway ◽  
Transcriptional Coactivator ◽  
Breast Cancer Patients ◽  
Poor Survival ◽  
Protein Levels ◽  
The Hippo Pathway

YAP1 plays a key role as a transcriptional coactivator in the Hippo pathway. Based on conflicting reports regarding YAP1 function in cancer, this study discerned its role in breast carcinogenesis. First, a systematic review of salient breast cancer studies targeting YAP1 dysregulation was performed. Additionally, freshly excised tumor specimens of approximately 200 breast cancer patients were processed for quantification of YAP1 expression at mRNA and protein levels using quantitative PCR and immunohistochemistry, respectively. YAP1 expression was nine folds higher in tumors versus controls and significantly associated with metastasis (p < 0.05) and poor survival in Pakistani breast cancer patients. These findings establish the role of YAP1 overexpression in tumorigenesis and metastasis. Hence, YAP1 inhibition may be considered a possible therapeutic strategy.

scholarly journals Gremlin-1 Promotes Metastasis of Breast Cancer Cells by Activating STAT3-MMP13 Signaling Pathway

2020 ◽  
Vol 21 (23) ◽  
pp. 9227
Author(s):  
Nam Ji Sung ◽  
Na Hui Kim ◽  
Young-Joon Surh ◽  
Sin-Aye Park
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Lung Metastasis ◽  
Cancer Progression ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Migration And Invasion ◽  
Breast Cancer Patients ◽  
Gremlin 1

Gremlin-1 (GREM1), one of the bone morphogenetic protein (BMP) antagonists, can directly bind to BMPs. GREM1 is involved in organogenesis, tissue differentiation, and organ fibrosis. Recently, numerous studies have reported the oncogenic role of GREM1 in cancer. However, the role of GREM1 in metastasis of breast cancer cells and its underlying mechanisms remain poorly understood. The role of GREM1 in breast cancer progression was assessed by measuring growth, migration, and invasion of breast cancer cells. An orthotopic breast cancer mouse model was used to investigate the role of GREM1 in lung metastasis of breast cancer cells. GREM1 knockdown suppressed the proliferation of breast cancer cells, while its overexpression increased their growth, migration, and invasion. Cells with Grem1-knockdown showed much lower tumor growth rates and lung metastasis than control cells. GREM1 enhanced the expression of matrix metalloproteinase 13 (MMP13). A positive correlation between GREM1 and MMP13 expression was observed in breast cancer patients. GREM1 activated signal transducer and activator of transcription 3 (STAT3) transcription factor involved in the expression of MMP13. Our study suggests that GREM1 can promote lung metastasis of breast cancer cells through the STAT3-MMP13 pathway. In addition, GREM1 might be a promising therapeutic target for breast cancer metastasis.

scholarly journals Activation of PI3K/AKT/mTOR Pathway Causes Drug Resistance in Breast Cancer

2021 ◽  
Vol 12 ◽  
Author(s):  
Chao Dong ◽  
Jiao Wu ◽  
Yin Chen ◽  
Jianyun Nie ◽  
Ceshi Chen
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Progression ◽  
Critical Role ◽  
Acquired Resistance ◽  
Mtor Inhibitors ◽  
Disease Recurrence ◽  
Mtor Pathway ◽  
Breast Cancer Patients

Although chemotherapy, targeted therapy and endocrine therapy decrease rate of disease recurrence in most breast cancer patients, many patients exhibit acquired resistance. Hyperactivation of the PI3K/AKT/mTOR pathway is associated with drug resistance and cancer progression. Currently, a number of drugs targeting PI3K/AKT/mTOR are being investigated in clinical trials by combining them with standard therapies to overcome acquired resistance in breast cancer. In this review, we summarize the critical role of the PI3K/AKT/mTOR pathway in drug resistance, the development of PI3K/AKT/mTOR inhibitors, and strategies to overcome acquired resistance to standard therapies in breast cancer.

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