scholarly journals miR-183-5p Aggravates Breast Cancer Development via Mediation of RGS2

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Chihua Wu ◽  
Youlin Tuo ◽  
Gang Hu ◽  
Jing Luo
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Regulatory Gene ◽  
Cancer Development ◽  
Luciferase Assay ◽  
Cancer Targeting ◽  
Cancer Tissue ◽  
Breast Cancer Development ◽  
Functional Assays ◽  
Promising Target

This study mainly explores how miR-183-5p pertains to breast cancer (BC) development. Functional assays were employed to test impacts of miR-183-5p in this cancer. Targeting between RGS2 and miR-183-5p was examined with dual-luciferase assay, and how their interaction pertains to cancer progression was further unraveled. miR-183-5p level was noticeably high in cancer tissue/cells. Overexpressing miR-183-5p could remarkably deteriorate cancer progression. The regulatory gene RGS2 levels was markedly low in BC, and two genes we researched were negatively correlated. It was uncovered by rescue assay that miR-183-5p/RGS2 axis mediated tumor-relevant behaviors in BC. Altogether, miR-183-5p aggravates BC development via mediation of RGS2. miR-183-5p supplies a promising target for BC therapy.

scholarly journals Role of extracellular matrix in breast cancer development: a brief update

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 274 ◽  
Author(s):  
Manoj Kumar Jena ◽  
Jagadeesh Janjanam
Keyword(s):  
Breast Cancer ◽  
Extracellular Matrix ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Cancer Development ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Breast Cancer Development ◽  
Cancer Pathogenesis

Evidence is increasing on the crucial role of the extracellular matrix (ECM) in breast cancer progression, invasion and metastasis with almost all mortality cases owing to metastasis. The epithelial-mesenchymal transition is the first signal of metastasis involving different transcription factors such as Snail, TWIST, and ZEB1. ECM remodeling is a major event promoting cancer invasion and metastasis; where matrix metalloproteinases (MMPs) such as MMP-2, -9, -11, and -14 play vital roles degrading the matrix proteins for cancer spread. The β-D mannuronic acid (MMP inhibitor) has anti-metastatic properties through inhibition of MMP-2, and -9 and could be a potential therapeutic agent. Besides the MMPs, the enzymes such as LOXL2, LOXL4, procollagen lysyl hydroxylase-2, and heparanase also regulate breast cancer progression. The important ECM proteins like integrins (b1-, b5-, and b6- integrins), ECM1 protein, and Hic-5 protein are also actively involved in breast cancer development. The stromal cells such as tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and adipocytes also contribute in tumor development through different processes. The TAMs become proangiogenic through secretion of VEGF-A and building vessel network for nourishment and invasion of the tumor mass. The latest developments of ECM involvement in breast cancer progression has been discussed in this review and this study will help researchers in designing future work on breast cancer pathogenesis and developing therapy targeted to the ECM components.

scholarly journals Role of extracellular matrix in breast cancer development: a brief update

F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 274 ◽  
Author(s):  
Manoj Kumar Jena ◽  
Jagadeesh Janjanam
Keyword(s):  
Breast Cancer ◽  
Extracellular Matrix ◽  
Cancer Progression ◽  
Breast Cancer Progression ◽  
Cancer Development ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Breast Cancer Development ◽  
Cancer Pathogenesis

Evidence is increasing on the crucial role of the extracellular matrix (ECM) in breast cancer progression, invasion and metastasis with almost all mortality cases owing to metastasis. The epithelial-mesenchymal transition is the first signal of metastasis involving different transcription factors such as Snail, TWIST, and ZEB1. ECM remodeling is a major event promoting cancer invasion and metastasis; where matrix metalloproteinases (MMPs) such as MMP-2, -9, -11, and -14 play vital roles degrading the matrix proteins for cancer spread. The β-D mannuronic acid (MMP inhibitor) has anti-metastatic properties through inhibition of MMP-2, and -9 and could be a potential therapeutic agent. Besides the MMPs, the enzymes such as LOXL2, LOXL4, procollagen lysyl hydroxylase-2, and heparanase also regulate breast cancer progression. The important ECM proteins like integrins (b1-, b5-, and b6- integrins), ECM1 protein, and Hic-5 protein are also actively involved in breast cancer development. The stromal cells such as tumor-associated macrophages (TAMs), cancer-associated fibroblasts (CAFs), and adipocytes also contribute in tumor development through different processes. The TAMs become proangiogenic through secretion of VEGF-A and building vessel network for nourishment and invasion of the tumor mass. The latest developments of ECM involvement in breast cancer progression has been discussed in this review and this study will help researchers in designing future work on breast cancer pathogenesis and developing therapy targeted to the ECM components.

scholarly journals Role of microRNAs in breast cancer development and their potential as biomarkers

2018 ◽  
Vol 14 (3) ◽  
pp. 40-47 ◽  
Author(s):  
K. A. Grishina ◽  
V. A. Khaylenko ◽  
D. V. Khaylenko ◽  
A. V. Karpukhin
Keyword(s):  
Breast Cancer ◽  
Cancer Progression ◽  
Malignant Disease ◽  
Molecular Mechanisms ◽  
Develop Breast Cancer ◽  
Cancer Prognosis ◽  
Cancer Development ◽  
Targeted Drugs ◽  
Breast Cancer Development

Breast cancer is the 2nd most common malignant disease after lung cancer; about 1 in 8 women will develop breast cancer in her lifetime. Cancer progression is a serious complication of the disease that encourages comprehensive investigation of molecular mechanisms underlying breast cancer development. This is also important for healthcare professionals involved in patient management, since they have to choose an optimal treatment regimen. This article discusses the role of microRNAs in the development of breast cancer, their biogenesis, classification, association with various molecular subtypes of breast cancer, and their potential role in the development of new targeted drugs for breast cancer therapy. Current research on the role of microRNAs in breast cancer progression is focused on the development of markers for breast cancer prognosis, diagnostic markers and new targeted drugs.

scholarly journals Cooperation of tissue factor cytoplasmic domain and PAR2 signaling in breast cancer development

Blood ◽  
2010 ◽  
Vol 116 (26) ◽  
pp. 6106-6113 ◽  
Author(s):  
Florence Schaffner ◽  
Henri H. Versteeg ◽  
Anja Schillert ◽  
Naho Yokota ◽  
Lars C. Petersen ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tissue Factor ◽  
Cancer Progression ◽  
Constitutive Expression ◽  
Close Correlation ◽  
Cytoplasmic Domain ◽  
Cancer Development ◽  
Coagulation Cascade ◽  
Breast Cancer Development ◽  
Angiogenic Switch

Abstract Constitutive expression of tissue factor (TF) by cancer cells triggers local activation of the coagulation cascade and promotes breast cancer progression through cell signaling involving protease activated receptor (PAR)2. In human breast cancer, TF and PAR2 are up-regulated and TF cytoplasmic domain phosphorylation is correlated with relapse. Here we show that cancer cell PAR2 signaling promotes angiogenesis independent of PAR2 phosphorylation at the recognized β-arrestin recruitment site. Similar to PAR2−/− mice, TF cytoplasmic domain–deleted (TFΔCT) mice have delayed spontaneous breast cancer development in the polyoma middle T model. Simultaneous deletion of PAR2 in TFΔCT mice did not further delay tumor appearance, consistent with overlapping roles of TF and PAR2 in promoting the angiogenic switch in early stages of breast cancer. In advanced carcinomas, tumor-associated macrophages were reduced in TFΔCT and TFΔCT/PAR2−/− mice, and increased tumor vessel diameters of TFΔCT mice were partially reversed by PAR2-deficiency, indicating that the TF cytoplasmic domain has additional roles that are interdependent with PAR2 signaling in regulating host angiogenic responses. These experiments demonstrate a crosstalk of tumor cell TF cytoplasmic domain and PAR2 signaling and provide a possible mechanism for the close correlation between TF phosphorylation and cancer recurrence of TF and PAR2-positive clinical breast cancer.

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