scholarly journals The gene expression landscape of breast cancer is shaped by tumor protein p53 status and epithelial-mesenchymal transition

2012 ◽  
Vol 14 (4) ◽  
Author(s):  
Erik Fredlund ◽  
Johan Staaf ◽  
Juha K Rantala ◽  
Olli Kallioniemi ◽  
Åke Borg ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Protein P53 ◽  
Tumor Protein P53 ◽  
P53 Status

scholarly journals Mummy Induces Apoptosis Through Inhibiting of Epithelial-Mesenchymal Transition (EMT) in Human Breast Cancer Cells

2020 ◽  
Vol 9 ◽  
pp. 1812
Author(s):  
Solmaz Rahmani Barouji ◽  
Arman Shahabi ◽  
Mohammadali Torbati ◽  
Seyyed Mohammad Bagher Fazljou ◽  
Ahmad Yari Khosroushahi
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Control Group ◽  
Mrna Levels ◽  
Mesenchymal Transition ◽  
Mcf 7

Background: Mummy (Iranian pure shilajit) is a remedy with possessing anti-inflammatory, antioxidant and anticancer activities. This study aimed to examine mummy effects on epithelial-mesenchymal transition (EMT) and invasiveness of MCF-7 and MDA-MB-231 breast cancer (BC) cell lines with underlying its mechanism. Materials and Methods: The dose-dependent inhibitory effect of the mummy on cell proliferation in vitro was determined using the MTT assay.  Flow cytometry and 4’,6-diamidino-2-phenylindole dihydrochloride staining were respectively used for quantitative and qualitative analysis of cellular apoptosis, and gene expression analysis was conducted using real-time PCR. Results: MDA-MB-231 showed more sensitivity than the MCF-7 cell line to the anticancer activity of mummy, while mummy did not exhibit significant cell cytotoxicity against human normal cells (MCF-10A). The gene expression profile demonstrated a significant decrease in TGF-β1, TGF-βR1, TWIST1, NOTCH1, CTNNB1, SRC along with an increase in E-cadherin mRNA levels in mummy treated cells compared to the untreated control group (P≤0.05). Conclusion: Mummy triggers inhibition of EMT and metastasis in breast cancer cells mainly through the downregulation of TGFβ1 activity, and more studies required to find its specific anticancer activity with details. [GMJ.2020;9:e1812]

scholarly journals An unsupervised feature extraction and selection strategy for identifying epithelial-mesenchymal transition state metrics in breast cancer and melanoma

2019 ◽  
Author(s):  
David J. Klinke ◽  
Arezo Torang
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Tumor Microenvironment ◽  
Epithelial Mesenchymal Transition ◽  
Cell Phenotype ◽  
Holistic View ◽  
Mesenchymal Transition ◽  
Feature Extraction And Selection ◽  
Cellular Context ◽  
Immune Contexture

Digital cytometry is opening up new avenues to better understand the heterogeneous cell types present within the tumor microenvironment. While the focus is towards elucidating immune and stromal cells as clinical correlates, there is still a need to better understand how a change in tumor cell phenotype, such as the epithelial-mesenchymal transition, influences the immune contexture. To complement existing digital cytometry methods, our objective was to develop an unsupervised gene signature capturing a change in differentiation state that is tailored to the specific cellular context of breast cancer and melanoma, as a illustrative example. Towards this aim, we used principal component analysis coupled with resampling to develop unsupervised gene expression-based state metrics specific for the cellular context that characterize the state of cellular differentiation within an epithelial to mesenchymal-like state space and independently correlate with metastatic potential. First developed using cell line data, the orthogonal state metrics were refined to exclude the contributions of normal fibroblasts and to provide tissue-level state estimates based on bulk tissue RNA-seq measures. The resulting gene expression-based metrics for differentiation state aim to inform a more holistic view of how the malignant cell phenotype influences the immune contexture within the tumor microenvironment.

scholarly journals Contribution of miRNAs in the Pathogenesis of Breast Cancer

2021 ◽  
Vol 11 ◽  
Author(s):  
Soudeh Ghafouri-Fard ◽  
Ali Khanbabapour Sasi ◽  
Atefe Abak ◽  
Hamed Shoorei ◽  
Ali Khoshkar ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Expression Profiling ◽  
Epithelial Mesenchymal Transition ◽  
Breast Carcinogenesis ◽  
Mesenchymal Transition ◽  
Non Invasive ◽  
Heterogeneous Nature ◽  
Almost All ◽  
Resistance To Chemotherapy

Breast cancer is the most frequently diagnosed cancer among females. Gene expression profiling methods have shown the deregulation of several genes in breast cancer samples and have confirmed the heterogeneous nature of breast cancer at the genomic level. microRNAs (miRNAs) are among the recently appreciated contributors in breast carcinogenic processes. These small-sized transcripts have been shown to partake in breast carcinogenesis through modulation of apoptosis, autophagy, and epithelial–mesenchymal transition. Moreover, they can confer resistance to chemotherapy. Based on the contribution of miRNAs in almost all fundamental aspects of breast carcinogenesis, therapeutic intervention with their expression might affect the course of this disorder. Moreover, the presence of miRNAs in the peripheral blood of patients potentiates these transcripts as tools for non-invasive diagnosis of breast cancer.

scholarly journals Adipocyte hypoxia promotes epithelial-mesenchymal transition-related gene expression and estrogen receptor-negative phenotype in breast cancer cells

2015 ◽  
Vol 33 (6) ◽  
pp. 2689-2694 ◽  
Author(s):  
AIWEI YAO-BORENGASSER ◽  
BEHJATOLAH MONZAVI-KARBASSI ◽  
REBECCA A HEDGES ◽  
LORA J ROGERS ◽  
SUSAN A KADLUBAR ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Estrogen Receptor ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Epithelial Mesenchymal Transition ◽  
Related Gene ◽  
Mesenchymal Transition ◽  
Estrogen Receptor Negative ◽  
Negative Phenotype

scholarly journals The role of miRNA in regulation of AXL, DAPK1, NFIB gene expression in breast cancer

2018 ◽  
pp. 130-133
Author(s):  
И.В. Пронина ◽  
Е.А. Филиппова ◽  
С.С. Лукина ◽  
А.М. Бурденный ◽  
Т.П. Казубская ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Epithelial Mesenchymal Transition ◽  
Negative Regulator ◽  
Protein Coding ◽  
Mesenchymal Transition ◽  
Protein Encoding ◽  
Apoptotic Pathways ◽  
Encoding Genes

Рак молочной железы (РМЖ) характеризуется эпигенетическими нарушениями, которые приводят к нарушению регуляции экспрессии опухоль ассоциированных белок-кодирующих генов, что влияет на развитие опухоли. Цель исследования - поиск новых микроРНК, потенциально вовлеченных в регуляцию экспрессии 3 белок-кодирующих генов (AXL, DAPK1, NFIB), связанных с регуляцией апоптоза и эпителиально-мезенхимального перехода при РМЖ. Методом количественной ПЦР определены изменения экспрессии 3 белок-кодирующих генов (AXL, DAPK1, NFIB) и 3 микроРНК (miR-127-5p, -132-3р, -9-5p), предсказанных с помощью алгоритмов miRWalk 2.0 как регуляторные. Определены статистически значимые отрицательные корреляции между изменениями уровней экспрессии микроРНК и мРНК для следующих пар: miR-127-5p - DAPK1 (Rs = -0,503, p = 0,001) и miR-9-5p - DAPK1 (Rs = -0,335, p = 0,040). Таким образом, установлена потенциальная роль двух микроРНК в регуляции экспрессии гена DAPK1, активатора различных путей апоптоза и негативного регулятора ЭМП, что имеет фундаментальное значение и может найти применение для разработки таргетной терапии РМЖ. Breast cancer (BC) is characterized by epigenetic disorders, which lead to dysregulation of protein-coding gene expression; together these result in development of a tumor. The goal of the study was to search for new miRNAs that are potentially involved in regulation of the expression of three protein-encoding genes (AXL, DAPK1, NFIB) associated with regulation of apoptosis and the epithelial-mesenchymal transition in breast cancer. Quantitative PCR was used to determine changes in the expression of three protein-coding genes (AXL, DAPK1, NFIB) and three miRNAs (miR-127-5p, -132-3p, -9-5p) that had been predicted to be regulators by miRWalk 2.0 algorithms. Statistically significant negative correlations between changes in miRNA and mRNA expression were determined for the following pairs: miR-127-5p - DAPK1 (Rs = -0.503, p = 0.001) and miR-9-5p - DAPK1 (Rs = -0.335, p = 0.040). Therefore, the study showed a potential role of two miRNAs in regulation of the DAPK1 gene expression, an activator of various apoptotic pathways and a negative regulator of EMT. This result is fundamentally important and can be used to develop targeted therapies for breast cancer.

scholarly journals Uev1A promotes breast cancer cell migration by up-regulating CT45A expression via the AKT pathway

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tong Niu ◽  
Zhaojia Wu ◽  
Wei Xiao
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cell Migration ◽  
Cancer Cell ◽  
Epithelial Mesenchymal Transition ◽  
Ectopic Expression ◽  
Cancer Cell Line ◽  
Colorectal Cancer Cell Line ◽  
Akt Pathway ◽  
Mesenchymal Transition

Abstract Background UEV1A encodes a ubiquitin-E2 variant closely associated with tumorigenesis and metastasis, but its underlying mechanism in promoting metastasis remains to be investigated. Methods In this study, we experimentally manipulated UEV1A and CT45A gene expression and monitored their effects on cancer-related gene expression, cell migration and the signal transduction cascade. Results It was found that UEV1A overexpression induces CT45A family gene expression in breast cancer cells. Indeed, ectopic expression of UEV1A was sufficient to induce CT45A and its downstream genes involved in tumorigenesis, epithelial-mesenchymal transition (EMT), stemness and metastasis, and to promote cell migration and EMT signaling. Consistently, depletion of CT45A abolished the above effects, indicating that CT45A is a critical downstream effector of Uev1A. The Uev1A-induced cell migration and EMT signaling was dependent on AKT but independent of NF-κB, indicating that CT45A acts downstream of the AKT pathway. Conclusions Based on previous reports and observations in this study, we propose that the Ubc13-Uev1A complex activates AKT through K63-linked polyubiquitination, which leads to enhanced CT45A expression, stimulated cell migration and EMT signaling in breast cells. Since similar effects were also observed in a colorectal cancer cell line, the Ubc13/Uev1A-AKT-CT45A axis may also promote tumorigenesis and metastasis in other tissues.

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