Proteomic Analysis of Colorectal Cancer Metastasis: Stathmin-1 Revealed as a Player in Cancer Cell Migration and Prognostic Marker

2012 ◽  
Vol 11 (2) ◽  
pp. 1433-1445 ◽  
Author(s):  
Hwee Tong Tan ◽  
Wei Wu ◽  
Yi Zhen Ng ◽  
Xuxiao Zhang ◽  
Benedict Yan ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Prognostic Marker ◽  
Cancer Cell ◽  
Proteomic Analysis ◽  
Cancer Metastasis ◽  
Cancer Cell Migration ◽  
Stathmin 1 ◽  
Colorectal Cancer Metastasis

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.

scholarly journals TGF‐β‐induced IGFBP‐3 is a key paracrine factor from activated pericytes that promotes colorectal cancer cell migration and invasion

2020 ◽  
Vol 14 (10) ◽  
pp. 2609-2628 ◽  
Author(s):  
Rocío Navarro ◽  
Antonio Tapia‐Galisteo ◽  
Laura Martín‐García ◽  
Carlos Tarín ◽  
Cesáreo Corbacho ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Colorectal Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Paracrine Factor ◽  
Cell Migration And Invasion ◽  
Igfbp 3

scholarly journals Overexpression of lncRNA NLIPMT Inhibits Colorectal Cancer Cell Migration and Invasion by Downregulating TGF-β1

2020 ◽  
Vol Volume 12 ◽  
pp. 6045-6052
Author(s):  
Yongkang An ◽  
Shuangxi Zhang ◽  
Jing Zhang ◽  
Qing Yin ◽  
Haitao Han ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Migration ◽  
Cancer Cell ◽  
Colorectal Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Migration ◽  
Cell Migration And Invasion ◽  
Tgf Β1

scholarly journals Comparative mechanisms of cancer cell migration through 3D matrix and physiological microtracks

2015 ◽  
Vol 308 (6) ◽  
pp. C436-C447 ◽  
Author(s):  
Shawn P. Carey ◽  
Aniqua Rahman ◽  
Casey M. Kraning-Rush ◽  
Bethsabe Romero ◽  
Sahana Somasegar ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Actin Polymerization ◽  
Cancer Metastasis ◽  
Type I Collagen ◽  
Type I ◽  
Cancer Cell Migration ◽  
Cytoskeletal Dynamics ◽  
3D Matrix ◽  
Context Specific

Tumor cell invasion through the stromal extracellular matrix (ECM) is a key feature of cancer metastasis, and understanding the cellular mechanisms of invasive migration is critical to the development of effective diagnostic and therapeutic strategies. Since cancer cell migration is highly adaptable to physiochemical properties of the ECM, it is critical to define these migration mechanisms in a context-specific manner. Although extensive work has characterized cancer cell migration in two- and three-dimensional (3D) matrix environments, the migration program employed by cells to move through native and cell-derived microtracks within the stromal ECM remains unclear. We previously reported the development of an in vitro model of patterned type I collagen microtracks that enable matrix metalloproteinase-independent microtrack migration. Here we show that collagen microtracks closely resemble channel-like gaps in native mammary stroma ECM and examine the extracellular and intracellular mechanisms underlying microtrack migration. Cell-matrix mechanocoupling, while critical for migration through 3D matrix, is not necessary for microtrack migration. Instead, cytoskeletal dynamics, including actin polymerization, cortical tension, and microtubule turnover, enable persistent, polarized migration through physiological microtracks. These results indicate that tumor cells employ context-specific mechanisms to migrate and suggest that selective targeting of cytoskeletal dynamics, but not adhesion, proteolysis, or cell traction forces, may effectively inhibit cancer cell migration through preformed matrix microtracks within the tumor stroma.

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