scholarly journals Overexpression of the RNA binding protein HuR impairs tumor growth in triple negative breast cancer associated with deficient angiogenesis

Cell Cycle ◽  
2010 ◽  
Vol 9 (16) ◽  
pp. 3357-3366 ◽  
Author(s):  
Matthew M Gubin ◽  
Robert Calaluce ◽  
Justin Wade Davis ◽  
Joseph D Magee ◽  
Connie S. Strouse ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tumor Growth ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein

Abstract 3271: The RNA binding protein HuR controls angiogenesis in triple negative breast cancer

2010 ◽  
Author(s):  
Ulus Atasoy ◽  
Matthew Gubin ◽  
Bob Calaluce ◽  
Wade Davis ◽  
Joseph Magee ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein

Abstract 3084: The role of RNA-binding protein HuR in lung metastasis of triple-negative breast cancer

2011 ◽  
Author(s):  
Patsharaporn Techasintana ◽  
Matthew Michael Gubin ◽  
Joseph David Magee ◽  
Garrett MacKenzie Dahm ◽  
Ulus Atasoy
Keyword(s):  
Breast Cancer ◽  
Lung Metastasis ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein

Long non-coding RNA LINC-PINT attenuates paclitaxel resistance in triple-negative breast cancer cells via targeting the RNA-binding protein NONO

2020 ◽  
Vol 52 (8) ◽  
pp. 801-809 ◽  
Author(s):  
Jinghua Chen ◽  
Meiqin Zhu ◽  
Liqiu Zou ◽  
Junxian Xia ◽  
Jiacheng Huang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Triple Negative Breast Cancer ◽  
Triple Negative ◽  
Rna Binding ◽  
Binding Protein ◽  
Rna Binding Protein ◽  
Non Coding Rna ◽  
Long Non Coding Rna

Abstract The treatment of triple-negative breast cancer (TNBC) relies largely on chemotherapies. However, it is frequent that TNBC patients develop resistance to the chemotherapy drugs. Generation of drug-resistant cell lines facilitates the identification of drug resistance. Here, we established two paclitaxel (PTX)-resistant TNBC cancer cell lines using an intermittent and stepwise method and found that long non-coding RNA long intergenic non-protein-coding RNA p53-induced transcript (LINC-PINT) was significantly decreased in PTX-resistant cancer cells. Ectopic expression of LINC-PINT sensitized both PTX-resistant TNBC and wild-type TNBC to PTX. Moreover, RNA immunoprecipitation showed that LINC-PINT bound to RNA-binding protein NONO. Overexpression of LINC-PINT resulted in the degradation of NONO in a proteasome-dependent manner and vice versa. Knockdown of NONO with siRNA sensitized TNBC to PTX. We further analyzed the expression level of LINC-PINT and NONO in patient samples via online database and found that LINC-PINT and NONO may function antagonistically in all types of breast cancers. Taken together, our data illustrated a tumor suppressor role of LINC-PINT in sensitizing TNBC to chemotherapies via destabilizing NONO.

Effect of RNA-binding protein MSI2 deficiency on progression in triple-negative breast cancer via stabilizing TP53INP1.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e12555-e12555
Author(s):  
Ping Wei ◽  
Ming Li ◽  
Wentao Yang ◽  
Xiaoyan Zhou
Keyword(s):  
Breast Cancer ◽  
Triple Negative Breast Cancer ◽  
Cell Invasion ◽  
Triple Negative ◽  
Rna Binding ◽  
Rna Binding Protein ◽  
Normal Tissues ◽  
Tnbc Cell ◽  
Proliferation And Invasion

e12555 Background: The RNA-binding protein Musashi-2 (MSI2) has been implicated in the tumorigenesis and tumor progression of human cancers. This study investigated the clinical significance of MSI2 and the potential molecular mechanisms involved in triple-negative breast cancer (TNBC) progression. Methods: The Illumina sequencing platform was used to analyze the mRNA transcriptome in TNBC vs. normal tissues, while quantitative reverse transcription–polymerase chain reaction and immunohistochemistry validated MSI2 expression in breast cancer tissues and the effects of MSI2 on TNBC cells were assayed in vitro and in viv o. RNA immunoprecipitation (RIP) DNA and RNA sequencing was performed to identify the potential MSI2-targeted mRNAs. RIP and luciferase analyses were used to confirm the mRNA targets of MSI2. Results: MSI2 expression was significantly downregulated in TNBC vs. normal tissues and was associated with a poor overall survival of patients. MSI2 overexpression in vitro and in vivo inhibited TNBC cell proliferation and invasion as well as the extracellular signal-regulated kinase 1/2 (ERK1/2) activity. Molecularly, MSI2 expression promoted the stability of TP53INP1 mRNA by its interaction with the TP53INP1 mRNA 3ʹ-untranslated region. Furthermore, knockdown of TP53INP1 expression was able to reverse MSI2-induced suppression of TNBC cell invasion, whereas ectopic expression of TP53INP1 and inhibition of the ERK1/2 activity blocked MSI2 knockdown-induced TNBC cell invasion. Conclusions: The current study demonstrated that downregulated MSI2 expression was associated with TNBC progression and a poor prognosis and that MSI2 expression inhibited TNBC proliferation and invasion by induction of TP53INP1 stability and inhibition of ERK1/2 activity.

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