Downregulated miR-1247-5p associates with poor prognosis and facilitates tumor cell growth via DVL1/Wnt/β-catenin signaling in breast cancer

2018 ◽  
Vol 505 (1) ◽  
pp. 302-308 ◽  
Author(s):  
Beilei Zeng ◽  
Yunhai Li ◽  
Yixiao Feng ◽  
Mengqi Lu ◽  
Hongfan Yuan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Poor Prognosis ◽  
Tumor Cell Growth

scholarly journals DACT1, an antagonist to Wnt/β-catenin signaling, suppresses tumor cell growth and is frequently silenced in breast cancer

2013 ◽  
Vol 15 (2) ◽  
Author(s):  
Xuedong Yin ◽  
Tingxiu Xiang ◽  
LiLi Li ◽  
Xianwei Su ◽  
Xingsheng Shu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Tumor Cell Growth

Genistein induces breast cancer-associated aromatase and stimulates estrogen-dependent tumor cell growth in in vitro breast cancer model

Toxicology ◽  
2011 ◽  
Vol 289 (2-3) ◽  
pp. 67-73 ◽  
Author(s):  
M.B.M. van Duursen ◽  
S.M. Nijmeijer ◽  
E.S. de Morree ◽  
P. Chr. de Jong ◽  
M. van den Berg
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Tumor Cell Growth ◽  
Cancer Model ◽  
Breast Cancer Model

scholarly journals ROR1 Is Expressed in Human Breast Cancer and Associated with Enhanced Tumor-Cell Growth

PLoS ONE ◽  
2012 ◽  
Vol 7 (3) ◽  
pp. e31127 ◽  
Author(s):  
Suping Zhang ◽  
Liguang Chen ◽  
Bing Cui ◽  
Han-Yu Chuang ◽  
Jianqiang Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Human Breast Cancer ◽  
Tumor Cell Growth ◽  
Human Breast

scholarly journals LncRNA PVT1 Is a Poor Prognosticator and Can Be Targeted by PVT1 Antisense Oligos in Gastric Adenocarcinoma

Cancers ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2995
Author(s):  
Yuan Li ◽  
Shumei Song ◽  
Melissa Pool Pizzi ◽  
Guangchun Han ◽  
Ailing W. Scott ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Gastric Adenocarcinoma ◽  
Poor Prognosis ◽  
Survival Duration ◽  
Tumor Cell Growth ◽  
Normal Tissues ◽  
Antisense Oligos

Gastric adenocarcinoma (GAC) is inherently resistant or becomes resistant to therapy, leading to a poor prognosis. Mounting evidence suggests that lncRNAs can be used as predictive markers and therapeutic targets in the right context. In this study, we determined the role of lncRNA-PVT1 in GAC along with the value of inhibition of PVT1 using antisense oligos (ASOs). RNA scope in situ hybridization was used to analyze PVT1 expression in tumor tissue microarrays (TMAs) of GAC and paired normal tissues from 792 patients. Functional experiments, including colony formation and invasion assays, were performed to evaluate the effects of PVT1 ASO inhibition of PVT1 in vitro; patient-derived xenograft models were used to evaluate the anti-tumor effects of PVT1 ASOs in vivo. LncRNA-PVT1 was upregulated in GACs compared to the matched adjacent normal tissues in the TMA. LncRNA PVT1 expression was positively correlated with larger tumor size, deeper wall invasion, lymph node metastases, and short survival duration. Inhibition of PVT1 using PVT1 ASOs significantly suppressed tumor cell growth and invasion in vitro and in vivo. PVT1 expression was highly associated with poor prognosis in GAC patients and targeting PVT1 using PVT1 ASOs was effective at curtailing tumor cell growth in vitro and in vivo. Thus, PVT1 is a poor prognosticator as well as therapeutic target. Targeting PVT1 using PVT1 ASOs provides a novel therapeutic strategy for GAC.

Abstract 3868: ROR1 is expressed in human breast cancer and associated with enhanced tumor-cell growth

2012 ◽  
Author(s):  
Suping Zhang ◽  
Liguang Chen ◽  
Bing Cui ◽  
Han-Yu Chuang ◽  
Jianqiang Yu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Human Breast Cancer ◽  
Tumor Cell Growth ◽  
Human Breast

Abstract P1-07-25: SSA, a novel sulindac sulfide derivative, inhibits tumor cell growth and invasion in breast cancer

2015 ◽  
Author(s):  
Bin Yi ◽  
Xiangling Feng ◽  
Hong Chang ◽  
Ruixia Ma ◽  
Xiaoguo Zhang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Tumor Cell Growth ◽  
Sulindac Sulfide

scholarly journals Epigenetic targeting of neuropilin-1 prevents bypass signaling in drug-resistant breast cancer

Oncogene ◽  
2020 ◽  
Author(s):  
Ammara Abdullah ◽  
Saeed Salehin Akhand ◽  
Juan Sebastian Paez Paez ◽  
Wells Brown ◽  
Li Pan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Growth Factor ◽  
Cell Growth ◽  
Tumor Cell ◽  
Metastatic Disease ◽  
Kinase Inhibitors ◽  
Growth Factor Receptor ◽  
Drug Resistant ◽  
Tumor Cell Growth ◽  
Mesenchymal Transition

Abstract Human epidermal growth factor receptor 2 (HER2)-amplified breast cancers are treated using targeted antibodies and kinase inhibitors, but resistance to these therapies leads to systemic tumor recurrence of metastatic disease. Herein, we conducted gene expression analyses of HER2 kinase inhibitor-resistant cell lines as compared to their drug-sensitive counterparts. These data demonstrate the induction of epithelial–mesenchymal transition (EMT), which included enhanced expression of fibroblast growth factor receptor 1 (FGFR1) and axonal guidance molecules known as neuropilins (NRPs). Immunoprecipitation of FGFR1 coupled with mass spectroscopy indicated that FGFR1 forms a physical complex with NRPs, which is enhanced upon induction of EMT. Confocal imaging revealed that FGFR1 and NRP1 predominantly interact throughout the cytoplasm. Along these lines, short hairpin RNA-mediated depletion of NRP1, but not the use of NRP1-blocking antibodies, inhibited FGFR signaling and reduced tumor cell growth in vitro and in vivo. Our results further indicate that NRP1 upregulation during EMT is mediated via binding of the chromatin reader protein, bromodomain containing 4 (BRD4) in the NRP1 proximal promoter region. Pharmacological inhibition of BRD4 decreased NRP1 expression and ablated FGF-mediated tumor cell growth. Overall, our studies indicate that NRPs facilitate aberrant growth factor signaling during EMT-associated drug resistance and metastasis. Pharmacological combination of epigenetic modulators with FGFR-targeted kinase inhibitors may provide improved outcomes for breast cancer patients with drug-resistant metastatic disease.

scholarly journals Metastatic growth instructed by neutrophil-derived transferrin

2018 ◽  
Vol 115 (43) ◽  
pp. 11060-11065 ◽  
Author(s):  
Wei Liang ◽  
Qin Li ◽  
Napoleone Ferrara
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Cancer Metastasis ◽  
Metastatic Breast ◽  
Tumor Cell Growth ◽  
Gm Csf ◽  
Proteomic Approach ◽  
Metastatic Growth

The tumor-promoting functions of neutrophils have been mainly attributed to induction of tumor angiogenesis or suppression of anticancer immunity. However, a direct impact of neutrophils on tumor cell growth and metastasis remains largely uncharacterized. Here, we coupled a proteomic approach with a functional screen to interrogate the secretome of tumor-associated neutrophils. Surprisingly, the iron-transporting protein transferrin was identified as the major mitogen for tumor cells secreted by neutrophils. Depletion of neutrophils inhibited lung metastasis and transferrin production in the metastatic microenvironment. Deletion of transferrin receptor suppressed growth of lung-colonizing tumor cells. Also, media conditioned by neutrophils isolated from metastatic breast cancer patients stimulated growth of human breast cancer cells, an effect that was largely abolished by transferrin immunodepletion. We identified GM-CSF, which is produced primarily by tumor cells, as a selective inducer of de novo transferrin synthesis in neutrophils through the Jak/Stat5β pathway. GM-CSF neutralization or inhibition of Jak kinases curtailed neutrophil transferrin expression in vitro and in vivo as well as cancer metastasis. Thus, transferrin provides a mechanistic link between neutrophils and metastatic growth owing to the ability of tumor-infiltrating neutrophils to locally deliver this growth-promoting protein in response to GM-CSF stimulation. Our study identifies neutrophil-derived transferrin as a key regulator of metastatic tumor cell growth and a therapeutic target for antimetastatic treatment.

Genistein induces breast cancer-associated aromatase and stimulates estrogen-dependent tumor cell growth in in vitro breast cancer model

Toxicology ◽  
2011 ◽  
Vol 290 (2-3) ◽  
pp. 145-146
Author(s):  
Majorie B.M. van Duursen ◽  
Evelien E.J.W. Smeets ◽  
Sandra M. Nijmeijer ◽  
Paul Chr de Jong ◽  
Martin van den Berg
Keyword(s):  
Breast Cancer ◽  
Cell Growth ◽  
Tumor Cell ◽  
Tumor Cell Growth ◽  
Cancer Model ◽  
Breast Cancer Model
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