Collagenases in Breast Cancer Cell-Induced Metastatic Tumor Growth and Progression

2002 ◽  
Author(s):  
Nagarajan Selvamurugan
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Metastatic Tumor

scholarly journals Exosomes from Nischarin-Expressing Cells Reduce Breast Cancer Cell Motility and Tumor Growth

2019 ◽  
Vol 79 (9) ◽  
pp. 2152-2166 ◽  
Author(s):  
Mazvita Maziveyi ◽  
Shengli Dong ◽  
Somesh Baranwal ◽  
Ali Mehrnezhad ◽  
Rajamani Rathinam ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cell Motility ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Motility

scholarly journals Hemimethylation Patterns in Breast Cancer Cell Lines

2019 ◽  
Vol 18 ◽  
pp. 117693511987295 ◽  
Author(s):  
Shuying Sun ◽  
Yu Ri Lee ◽  
Brittany Enfield
Keyword(s):  
Breast Cancer ◽  
Dna Methylation ◽  
Tumor Growth ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Entire Genome ◽  
Cpg Sites

DNA methylation is an epigenetic event that involves adding a methyl group to the cytosine (C) site, especially the one that pairs with a guanine (G) site (ie, CG or CpG site), in a human genome. This event plays an important role in both cancerous and normal cell development. Previous studies often assume symmetric methylation on both DNA strands. However, asymmetric methylation, or hemimethylation (methylation that occurs only on 1 DNA strand), does exist and has been reported in several studies. Due to the limitation of previous DNA methylation sequencing technologies, researchers could only study hemimethylation on specific genes, but the overall genomic hemimethylation landscape remains relatively unexplored. With the development of advanced next-generation sequencing techniques, it is now possible to measure methylation levels on both forward and reverse strands at all CpG sites in an entire genome. Analyzing hemimethylation patterns may potentially reveal regions related to undergoing tumor growth. For our research, we first identify hemimethylated CpG sites in breast cancer cell lines using Wilcoxon signed rank tests. We then identify hemimethylation patterns by grouping consecutive hemimethylated CpG sites based on their methylation states, methylation “M” or unmethylation “U.” These patterns include regular (or consecutive) hemimethylation clusters (eg, “MMM” on one strand and “UUU” on another strand) and polarity (or reverse) clusters (eg, “MU” on one strand and “UM” on another strand). Our results reveal that most hemimethylation clusters are the polarity type, and hemimethylation does occur across the entire genome with notably higher numbers in the breast cancer cell lines. The lengths or sizes of most hemimethylation clusters are very short, often less than 50 base pairs. After mapping hemimethylation clusters and sites to corresponding genes, we study the functions of these genes and find that several of the highly hemimethylated genes may influence tumor growth or suppression. These genes may also indicate a progressing transition to a new tumor stage.

scholarly journals Non-canonical BAD activity regulates breast cancer cell and tumor growth via 14-3-3 binding and mitochondrial metabolism

Oncogene ◽  
2019 ◽  
Vol 38 (18) ◽  
pp. 3325-3339 ◽  
Author(s):  
Jasdeep Mann ◽  
John Maringa Githaka ◽  
Timothy W. Buckland ◽  
Ning Yang ◽  
Rachel Montpetit ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Mitochondrial Metabolism

scholarly journals Distinct roles for paxillin and Hic-5 in regulating breast cancer cell morphology, invasion, and metastasis

2011 ◽  
Vol 22 (3) ◽  
pp. 327-341 ◽  
Author(s):  
Nicholas O. Deakin ◽  
Christopher E. Turner
Keyword(s):  
Breast Cancer ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cell Morphology ◽  
Molecular Mechanisms ◽  
Adhesion Formation ◽  
Three Dimensional ◽  
Rho Kinase ◽  
Adaptor Protein ◽  
Metastatic Tumor

Individual metastatic tumor cells exhibit two interconvertible modes of cell motility during tissue invasion that are classified as either mesenchymal or amoeboid. The molecular mechanisms by which invasive breast cancer cells regulate this migratory plasticity have yet to be fully elucidated. Herein we show that the focal adhesion adaptor protein, paxillin, and the closely related Hic-5 have distinct and unique roles in the regulation of breast cancer cell lung metastasis by modulating cell morphology and cell invasion through three-dimensional extracellular matrices (3D ECMs). Cells depleted of paxillin by RNA interference displayed a highly elongated mesenchymal morphology, whereas Hic-5 knockdown induced an amoeboid phenotype with both cell populations exhibiting reduced plasticity, migration persistence, and velocity through 3D ECM environments. In evaluating associated signaling pathways, we determined that Rac1 activity was increased in cells devoid of paxillin whereas Hic-5 silencing resulted in elevated RhoA activity and associated Rho kinase–induced nonmuscle myosin II activity. Hic-5 was essential for adhesion formation in 3D ECMs, and analysis of adhesion dynamics and lifetime identified paxillin as a key regulator of 3D adhesion assembly, stabilization, and disassembly.

Quercetin conjugated with silica nanoparticles inhibits tumor growth in MCF-7 breast cancer cell lines

2018 ◽  
Vol 500 (4) ◽  
pp. 860-865 ◽  
Author(s):  
Fahimeh Aghapour ◽  
Ali Akbar Moghadamnia ◽  
Andrea Nicolini ◽  
Seydeh Narges Mousavi Kani ◽  
Ladan Barari ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Silica Nanoparticles ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Mcf 7

Matrix stiffness and cluster size collectively regulate dormancy versus proliferation in brain metastatic breast cancer cell clusters

2020 ◽  
Vol 8 (23) ◽  
pp. 6637-6646
Author(s):  
Raghu Vamsi Kondapaneni ◽  
Shreyas S. Rao
Keyword(s):  
Breast Cancer ◽  
Metastatic Breast Cancer ◽  
Tumor Cell ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cluster Size ◽  
Metastatic Breast ◽  
Metastatic Tumor ◽  
Matrix Stiffness ◽  
Cell Clusters

Dormant versus proliferative phenotypes in metastatic tumor cell clusters are mediated via matrix stiffness and cluster size.

scholarly journals Inhibitory effects of iron depletion plus eribulin on the breast cancer microenvironment

BMC Cancer ◽  
2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Wataru Goto ◽  
Shinichiro Kashiwagi ◽  
Yuka Asano ◽  
Koji Takada ◽  
Tamami Morisaki ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Iron Chelator ◽  
Immune Checkpoints ◽  
Mcf 7

Abstract Background Iron is required for the proliferation of cancer cells, and its depletion suppresses tumor growth. Eribulin mesylate (eribulin), a non-taxane microtubule inhibitor, disrupts the tumor microenvironment via vascular remodeling and obstruction of the epithelial-mesenchymal transition (EMT). Herein, we investigated the effects of the iron chelator on tumor-related properties of breast cancer cells and the effects of iron chelator plus eribulin on tumor growth in vivo. Methods Two triple-negative breast cancer (TNBC) cell lines, MDA-MB-231 and BT-549, and one hormone-receptor positive breast cancer cell line, MCF-7, were used in our study. Cell proliferation, cell migration, cell cycle position, and gene expression were analyzed via MTT assays, wound-healing assays, flow cytometry, and quantitative real-time-polymerase chain reaction, respectively. For the in vivo experiments, mice with breast cancer xenografts were treated with the inhibitors, alone or together, and tumor volume was determined. Results Iron chelator inhibited breast cancer cell proliferation and decreased the proportion of S-phase cells. Conversely, it induced hypoxia, angiogenesis, EMT, and immune checkpoints, as determined by quantifying the expression of marker mRNAs in MDA-MB-231 and MCF-7 cells. Eribulin suppressed the expression of the hypoxia and EMT related marker mRNAs in the presence of iron chelator. Iron chelator plus eribulin inhibited tumor growth in vivo to a greater extent than did either inhibitor alone. Conclusions Although iron chelator induces oncogenic events (hypoxia, angiogenesis, EMT, and immune checkpoints), it may be an effective treatment for breast cancer when administered in combination with eribulin.

scholarly journals Saussurea lappaClarke-Derived Costunolide Prevents TNFα-Induced Breast Cancer Cell Migration and Invasion by Inhibiting NF-κB Activity

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Youn Kyung Choi ◽  
Sung-Gook Cho ◽  
Sang-Mi Woo ◽  
Yee Jin Yun ◽  
Jeakyung Jo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Metastatic Breast ◽  
Migration And Invasion ◽  
Invasion And Migration ◽  
Breast Cancer Cell Growth

Saussurea lappaClarke (SLC) has been used as a traditional medicine in Korea, China, and Japan for the treatment of abdominal pain and tenesmus. Costunolide, a sesquiterpene lactone isolated from SLC, has diverse medicinal effects. However, the anticancer effects of costunolide are still unclear in breast cancer. In this study, we demonstrate that costunolide suppresses tumor growth and metastases of MDA-MB-231 highly metastatic human breast cancer cells via inhibiting TNFα-induced NF-κB activation. Costunolide inhibited MDA-MB-231 tumor growth and metastases without affecting body weights in thein vivomouse orthotopic tumor growth assays. In addition, costunolide inhibitedin vitroTNFα-induced invasion and migration of MDA-MB-231 cells. Costunolide further suppressed TNFα-induced NF-κB signaling activation, resulting in a reduced expression of MMP-9, a well-known NF-κB-dependent gene to mediate breast cancer cell growth and metastases. Therefore, we conclude that SLC and its derivative costunolide suppress breast cancer growth and metastases by inhibiting TNFα-induced NF-κB activation, suggesting that costunolide as well as SLC may be promising anticancer drugs, especially for metastatic breast cancer.

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