scholarly journals Sodium valproate inhibits MDA-MB-231 breast cancer cell migration by upregulating NM23H1 expression

2012 ◽  
Vol 11 (1) ◽  
pp. 77-86 ◽  
Author(s):  
G.-F. Li ◽  
T.-L. Qian ◽  
G.-S. Li ◽  
C.-X. Yang ◽  
M. Qin ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Sodium Valproate ◽  
Cancer Cell Migration ◽  
Breast Cancer Cell Migration

scholarly journals The manganese(III) porphyrin MnTnHex-2-PyP5+ modulates intracellular ROS and breast cancer cell migration: Impact on doxorubicin-treated cells

Redox Biology ◽  
2019 ◽  
Vol 20 ◽  
pp. 367-378 ◽  
Author(s):  
Ana Flórido ◽  
Nuno Saraiva ◽  
Sara Cerqueira ◽  
Nuno Almeida ◽  
Maddy Parsons ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Migration ◽  
Breast Cancer Cell Migration ◽  
Intracellular Ros

scholarly journals Development of JNK2-Selective Peptide Inhibitors That Inhibit Breast Cancer Cell Migration

2011 ◽  
Vol 6 (6) ◽  
pp. 658-666 ◽  
Author(s):  
Tamer S. Kaoud ◽  
Shreya Mitra ◽  
Sunbae Lee ◽  
Juliana Taliaferro ◽  
Michael Cantrell ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Peptide Inhibitors ◽  
Cancer Cell Migration ◽  
Breast Cancer Cell Migration

scholarly journals Uncovering the signaling landscape controlling breast cancer cell migration identifies splicing factor PRPF4B as a metastasis driver

2018 ◽  
Author(s):  
Michiel Fokkelman ◽  
Esmee Koedoot ◽  
Vasiliki-Maria Rogkoti ◽  
Sylvia E. Le Dévédec ◽  
Iris van de Sandt ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Metastasis ◽  
Breast Cancer Cell Lines ◽  
Cancer Cell Migration ◽  
Metastasis Formation ◽  
Breast Cancer Cell Migration ◽  
Basal Breast Cancer

AbstractMetastasis is the major cause of death in cancer patients and migration of cancer cells from the primary tumor to distant sites is the prerequisite of metastasis formation. Here we applied an imaging-based RNAi phenotypic cell migration screen using two highly migratory basal breast cancer cell lines (Hs578T and MDA-MB-231) to provide a repository for signaling determinants that functionally drive cancer cell migration. We screened ~4,200 individual target genes covering most cell signaling components and discovered 133 and 113 migratory modulators of Hs578T and MDA-MB-231, respectively, of which 43 genes were common denominators of cell migration. Interaction networks of candidate migratory modulators were in common with networks of different clinical breast cancer prognostic and metastasis classifiers. The splicing factors PRPF4B and BUD31 and the transcription factor BPTF were amplified in human primary breast tumors and the expression was associated with metastasis-free survival. Depletion of PRPF4B, BUD31 and BPTF caused primarily down-regulation of genes involved in focal adhesion and ECM-interaction pathways. PRPF4B was essential for triple negative breast cancer cell migration and critical for breast cancer metastasis formation in vivo, making PRPF4B a candidate for further drug development. Our systematic phenotypic screen provides an important repository of candidate metastasis drug targets.

CXCL12-CXCL4 heterodimerization prevents CXCL12-driven breast cancer cell migration

2020 ◽  
Vol 66 ◽  
pp. 109488 ◽  
Author(s):  
Khanh T.P. Nguyen ◽  
Lawrence J. Druhan ◽  
Belinda R. Avalos ◽  
Li Zhai ◽  
Lubica Rauova ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Migration ◽  
Breast Cancer Cell Migration

scholarly journals Novel interactions between ERα-36 and STAT3 mediate breast cancer cell migration

2019 ◽  
Vol 17 (1) ◽  
Author(s):  
Yuan Xiang ◽  
Jia Peng Li ◽  
Wei Guo ◽  
Dan-Qun Wang ◽  
Ao Yao ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Migration ◽  
Breast Cancer Cell Migration ◽  
Novel Interactions

scholarly journals Acetylation of ezrin regulates membrane–cytoskeleton interaction underlying CCL18-elicited cell migration

2019 ◽  
Vol 12 (6) ◽  
pp. 424-437 ◽  
Author(s):  
Xiaoyu Song ◽  
Wanjuan Wang ◽  
Haowei Wang ◽  
Xiao Yuan ◽  
Fengrui Yang ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Lipid Binding ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion ◽  
Breast Cancer Cell Migration ◽  
Membrane Cytoskeleton

Abstract Ezrin, a membrane–cytoskeleton linker protein, plays an essential role in cell polarity establishment, cell migration, and division. Recent studies show that ezrin phosphorylation regulates breast cancer metastasis by promoting cancer cell survivor and promotes intrahepatic metastasis via cell migration. However, it was less characterized whether there are additional post-translational modifications and/or post-translational crosstalks on ezrin underlying context-dependent breast cancer cell migration and invasion. Here we show that ezrin is acetylated by p300/CBP-associated factor (PCAF) in breast cancer cells in response to CCL18 stimulation. Ezrin physically interacts with PCAF and is a cognate substrate of PCAF. The acetylation site of ezrin was mapped by mass spectrometric analyses, and dynamic acetylation of ezrin is essential for CCL18-induced breast cancer cell migration and invasion. Mechanistically, the acetylation reduced the lipid-binding activity of ezrin to ensure a robust and dynamic cycling between the plasma membrane and cytosol in response to CCL18 stimulation. Biochemical analyses show that ezrin acetylation prevents the phosphorylation of Thr567. Using atomic force microscopic measurements, our study revealed that acetylation of ezrin induced its unfolding into a dominant structure, which prevents ezrin phosphorylation at Thr567. Thus, these results present a previously undefined mechanism by which CCL18-elicited crosstalks between the acetylation and phosphorylation on ezrin control breast cancer cell migration and invasion. This suggests that targeting PCAF signaling could be a potential therapeutic strategy for combating hyperactive ezrin-driven cancer progression.

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