The role of GATA3 in breast cancer: An updated review

2021 ◽  
Vol 01 ◽  
Author(s):  
Jing Yang ◽  
Xu Zhao ◽  
Ruoyu Huang ◽  
Juanjuan Zhao ◽  
Mengmeng Guo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Target Genes ◽  
Treatment Strategies ◽  
Research Progress ◽  
Breast Cancer Patients ◽  
Exact Role ◽  
Promising Target ◽  
Mesenchymal Transformation

: GATA binding protein 3 (GATA3), a member of the zinc finger-binding transcription factor GATA gene family, plays an important role in regulating the development and differentiation of various tissues and organs. Previous studies have manifested that GATA3 is implicated in inhibiting the development of breast cancer, including suppressing the growth, metastasis and invasion of cancer cells. However, the exact role of GATA3 in breast cancer remains to be fully elucidated. Interestingly, recent studies have further shown that GATA3 can regulate a variety of new target genes including ectonucleoside triphosphate diphosphohydrolase 3 (ENTPD3), semaphorin 3B (SEMA3B) and microRNAs (miRNAs) to promote tumorgenisis, epithelial-mesenchymal transformation (EMT) and metastasis of breast cancer. Meanwhile, GATA3 mutations can affect the role of GATA3 in inhibiting the growth and metastasis of breast cancer cells, which indicates that GATA3 might be a promising target for breast cancer treatment. Undoubtedly, these new evidences further uncover the complexity of GATA3/targets network in breast cancer development. In this article, we review related research progress and put forward some questions about the development of GATA3 in future in order to be helpful for the understanding on the exact role of GATA3 in progress of breast cancer and the development of related new clinical treatment strategies that will ultimately benefit the clinical outcome of breast cancer 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.

miR-214 inhibits epithelial–mesenchymal transition of breast cancer cells via downregulation of RNF8

2019 ◽  
Vol 51 (8) ◽  
pp. 791-798 ◽  
Author(s):  
Lu Min ◽  
Chuanyang Liu ◽  
Jingyu Kuang ◽  
Xiaomin Wu ◽  
Lingyun Zhu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cancer Metastasis ◽  
Epithelial Mesenchymal Transition ◽  
Breast Cancer Metastasis ◽  
Breast Cancer Patients ◽  
Mesenchymal Transition ◽  
Proliferation And Invasion

Abstract MicroRNAs (miRNAs) are a class of endogenous noncoding genes that regulate gene expression at the posttranscriptional level. In recent decades, miRNAs have been reported to play important roles in tumor growth and metastasis, while some reported functions of a specific miRNA in tumorigenesis are contradictory. In this study, we reevaluated the role of miR-214, which has been reported to serve as an oncogene or anti-oncogene in breast cancer metastasis. We found that miR-214 inhibited breast cancer via targeting RNF8, a newly identified regulator that could promote epithelial–mesenchymal transition (EMT). Specifically, the survival rate of breast cancer patients was positively correlated with miR-214 levels and negatively correlated with RNF8 expression. The overexpression of miR-214 inhibited cell proliferation and invasion of breast cancer, while suppression of miR-214 by chemically modified antagomir enhanced the proliferation and invasion of breast cancer cells. Furthermore, miR-214 could modulate the EMT process via downregulating RNF8. To our knowledge, this is the first report that reveals the role of the miR-214–RNF8 axis in EMT, and our results demonstrate a novel mechanism for miR-214 acting as a tumor suppressor through the regulation of EMT.

Role of breast surgery in T1-T3 breast cancer patients with synchronous bone metastases.

2012 ◽  
Vol 30 (15_suppl) ◽  
pp. 1115-1115 ◽  
Author(s):  
Edoardo Botteri ◽  
Elisabetta Munzone ◽  
Vincenzo Bagnardi ◽  
Mattia Intra ◽  
Nicole Rotmensz ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Neoadjuvant Chemotherapy ◽  
Bone Metastases ◽  
Breast Surgery ◽  
Treatment Strategies ◽  
Surgical Margins ◽  
Her2 Overexpression ◽  
Breast Cancer Patients ◽  
Ki 67

1115 Background: The role of breast surgery in advanced breast cancer (ABC) is controversial. The main potential advantage of removing the primary tumor is to eliminate the source of further metastatic spread. While previous studies addressed the question in very heterogeneous populations (e.g. patients with any local and distant extension), we have focused on a homogeneous series of ABC patients. Methods: From our institutional Tumor Registry we selected 191 consecutive women diagnosed between 2000 and 2008 with locally operable (T1-T3) ABC, synchronous bone metastases and no other distant sites involved. The progression free survival (PFS) was calculated from diagnosis to the date of progression, defined as either a new site of metastatic disease or clinical/radiographic evidence of increasing tumor burden at a previously known bone metastatic site. Results: Median age was 51 years and 92% of the women had an endocrine-responsive tumor. One-hundred and thirty patients out of 191 (68%) underwent surgery at the time of diagnosis, while 61 (32%) did not. Twenty-six of the operated patients (20%) had previously undergone neoadjuvant chemotherapy; 15 (12%) had positive or undetermined surgical margins. Operated and non-operated patients were similar with respect to age, tumor size, nodal involvement, estrogen and progesterone receptor status, HER2 overexpression and Ki-67, but differed in terms of number of bone metastatic sites: a single metastasis was detected in 34 (26%) operated and 7 (11%) non-operated cases (P=0.02). First-line treatment strategies with endocrine therapy, chemotherapy and Trastuzumab were similarly distributed between the two groups. The 5-year PFS was 22.0% and 10.4% in operated and non-operated patients, respectively. The multi-adjusted hazard ratio was 0.62 (95% confidence interval 0.39-0.98) in favor of surgery. The exclusion of the patients who had received neoadjuvant chemotherapy and patients with positive or undetermined surgical margins did not alter the results. Conclusions: In this large and homogeneous series of ABC patients with synchronous bone metastases, the role of breast surgery had a favorable impact on the progression of the disease, indicating a potential survival benefit.

scholarly journals Exosomal miR-1246 is Involved in Tumorigenesis by Targeting THRB in Breast Cancer

2021 ◽  
Author(s):  
Jie Zhu ◽  
Xiaoying Chen ◽  
Fengxiang Xi ◽  
Lei Zhao ◽  
Yichao Wang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Target Genes ◽  
Metastatic Breast ◽  
Functional Enrichment ◽  
Breast Cancer Patients ◽  
Invasion And Migration ◽  
Kaplan Meier ◽  
Exosomal Mirnas ◽  
And Migration

Abstract Background: Exosomal miRNAs have drawn increasing attention as tumor biomarkers involving in tumorigenesis due to their stability. The aim of this study was to analyze the role of exosomal miR-1246 in breast cancer.Methods: The differentially expressed (DE) miRNAs in exosomes from the serum of breast cancer patients and healthy controls were investigated using RNA-seq. The potential pathogenic target genes and functional enrichment of these miRNAs were explored using bioinformatics. Additionally, the role of miR-1246 in migration, invasion and proliferation were investigated in breast cancer cells. The expression of THRB were detected by QRT-PCR. Kaplan-Meier plotter was used to perform survival analysis.Results: The results showed that the level of exosomal miR-1246 was significantly higher in breast cancer than in the control. MiR-1246 mimic treatment promoted invasion and migration in MDA-MB-231 cells by targeting THRB. Kaplan-Meier survival curves showed that patients with high miR-1246 expression exhibited poor OS compared with patients with low miR-1246 expression, especially those with metastatic breast cancer.Conclusion: Our study provides a better understanding of exosomal miR-1246 in the process of breast cancer. Exosomal miR-1246 could be a potential prognostic biomarker for breast carcinoma.

scholarly journals Update on the Role of Neuropeptide Y and Other Related Factors in Breast Cancer and Osteoporosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Shu-ting Lin ◽  
Yi-zhong Li ◽  
Xiao-qi Sun ◽  
Qian-qian Chen ◽  
Shun-fa Huang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Neuropeptide Y ◽  
Treatment Strategies ◽  
Nuclear Factor Κb ◽  
Breast Cancer Patients ◽  
Related Factors ◽  
Osteogenic Response ◽  
The Relationship

Breast cancer and osteoporosis are common diseases that affect the survival and quality of life in postmenopausal women. Women with breast cancer are more likely to develop osteoporosis than women without breast cancer due to certain factors that can affect both diseases simultaneously. For instance, estrogen and the receptor activator of nuclear factor-κB ligand (RANKL) play important roles in the occurrence and development of these two diseases. Moreover, chemotherapy and hormone therapy administered to breast cancer patients also increase the incidence of osteoporosis, and in recent years, neuropeptide Y (NPY) has also been found to impact breast cancer and osteoporosis.Y1 and Y5 receptors are highly expressed in breast cancer, and Y1 and Y2 receptors affect osteogenic response, thus potentially highlighting a potential new direction for treatment strategies. In this paper, the relationship between breast cancer and osteoporosis, the influence of NPY on both diseases, and the recent progress in the research and treatment of these diseases are reviewed.

scholarly journals Osterix Decreases the Chemosensitivity of Breast Cancer Cells by Upregulating GALNT14

2017 ◽  
Vol 44 (3) ◽  
pp. 998-1010 ◽  
Author(s):  
Jiahui Wu ◽  
Xiang Chen ◽  
Qianyi Bao ◽  
Rui Duan ◽  
Yucui Jin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Target Genes ◽  
Disease Free Survival ◽  
Breast Cancer Patients ◽  
Elevated Expression ◽  
Hoechst Staining

Background/Aims: Osterix (Osx), a key regulator of osteoblast differentiation and bone formation, has been recently reported to be associated with the progression of breast cancer. However, the precise roles of Osx in breast cancer remain unclear. Methods: Drug sensitivity of the cancer cells was assessed using an 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Target genes were obtained by high-throughput Illumina sequencing and were confirmed in vitro and in vivo. Apoptosis was analysed by Hoechst staining and western blotting. A tissue microarray including 129 samples from breast cancer patients was used for immunohistochemistry (IHC) assays. Results: Overexpression of Osx decreased the chemosensitivity of breast cancer cells, while knockdown of Osx increased the chemosensitivity of breast cancer cells. In particular, we found that the decreased chemosensitivity effect was significantly associated with elevated expression of the polypeptide N-acetylgalactosaminyltransferase 14 (GALNT14). Silencing of GALNT14 in Osx-overexpressed cells restored the decreased chemosensitivity. Conversely, overexpression of GALNT14 in Osx-knockdown cells abrogated the increased chemosensitivity in breast cancer cells. In addition, we revealed that Osx decreased GALNT14-dependent chemosensitivity by enhancing anti-apoptosis. GALNT14 expression exhibited a significant association with breast cancer stages as well as the disease-free survival (DFS) rate. Conclusion: Osx plays an important role in the chemosensitivity and inhibition of Osx expression may represent a therapeutic strategy to enhance the chemosensitivity of breast cancer.

scholarly journals The Epithelial to Mesenchymal Transition Promotes Glutamine Independence by Suppressing GLS2 Expression

Cancers ◽  
2019 ◽  
Vol 11 (10) ◽  
pp. 1610 ◽  
Author(s):  
Esmeralda Ramirez-Peña ◽  
James Arnold ◽  
Vinita Shivakumar ◽  
Robiya Joseph ◽  
Geraldine Vidhya Vijay ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial To Mesenchymal Transition ◽  
Treatment Strategies ◽  
Mitochondrial Activity ◽  
Breast Cancer Patients ◽  
Mesenchymal Transition ◽  
Metabolic Activities ◽  
New Treatment

Identifying bioenergetics that facilitate the epithelial to mesenchymal transition (EMT) in breast cancer cells may uncover targets to treat incurable metastatic disease. Metastasis is the number one cause of cancer-related deaths; therefore, it is urgent to identify new treatment strategies to prevent the initiation of metastasis. To characterize the bioenergetics of EMT, we compared metabolic activities and gene expression in cells induced to differentiate into the mesenchymal state with their epithelial counterparts. We found that levels of GLS2, which encodes a glutaminase, are inversely associated with EMT. GLS2 down-regulation was correlated with reduced mitochondrial activity and glutamine independence even in low-glucose conditions. Restoration of GLS2 expression in GLS2-negative breast cancer cells rescued mitochondrial activity, enhanced glutamine utilization, and inhibited stem-cell properties. Additionally, inhibition of expression of the transcription factor FOXC2, a critical regulator of EMT in GLS2-negative cells, restored GLS2 expression and glutamine utilization. Furthermore, in breast cancer patients, high GLS2 expression is associated with improved survival. These findings suggest that epithelial cancer cells rely on glutamine and that cells induced to undergo EMT become glutamine independent. Moreover, the inhibition of EMT leads to a GLS2-directed metabolic shift in mesenchymal cancer cells, which may make these cells susceptible to chemotherapies.

Deep learning of the role of interleukin IL-17 and its action in promoting cancer

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Alessandro Nutini ◽  
Ayesha Sohail
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Stochastic Modeling ◽  
Pathological Condition ◽  
Numerical Algorithms ◽  
Dynamical Analysis ◽  
Cell Populations ◽  
Breast Cancer Patients ◽  
High Level

AbstractIn breast cancer patients, metastasis remains a major cause of death. The metastasis formation process is given by an interaction between the cancer cells and the microenvironment that surrounds them. In this article, we develop a mathematical model that analyzes the role of interleukin IL-17 and its action in promoting cancer and in facilitating tissue metastasis in breast cancer, using a dynamic analysis based on a stochastic process that accounts for the local and global action of this molecule. The model uses the Ornstein–Uhlembeck and Markov process in continuous time. It focuses on the oncological expansion and the interaction between the interleukin IL-17 and cell populations This analysis tends to clarify the processes underlying the metastasis expansion mechanism both for a better understanding of the pathological event and for a possible better control of therapeutic strategies.IL-17 is a proinflammatory interleukin that acts when there is tissue damage or when there is a pathological situation caused by an external pathogen or by a pathological condition such as cancer.This research is focused on the role of interleukin IL-17 which, especially in the case of breast cancer, turns out to be a dominant “communication pin” since it interconnects with the activity of different cell populations affected by the oncological phenomenon. Stochastic modeling strategies, specially the Ornstein-Uhlenbeck process, with the aid of numerical algorithms are elaborated in this review.The role of IL-17 is discussed in this manuscript at all the stages of cancer. It is discussed that IL-17 also acts as “metastasis promoter” as a result of its proinflammatory nature. The stochastic nature of IL-17 is discussed based on the evidence provided by recent literature.The resulting dynamical analysis can help to select the most appropriate therapeutic strategy.Cancer cells, in the case of breast cancer, have high level of IL-17 receptors (IL-17R); therefore the interleukin itself has direct effects on these cells. Immunotherapy research, focused on this cytokine and interlinked with the stochastic modeling, seems to be a promising avenue.

Sign in / Sign up

Export Citation Format

Share Document