scholarly journals Role of RhoC in cancer cell migration

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Yingyue Lou ◽  
Yuhan Jiang ◽  
Zhen Liang ◽  
Bingzhang Liu ◽  
Tian Li ◽  
...  
Keyword(s):  
Cell Migration ◽  
Cancer Metastasis ◽  
Three Dimensional ◽  
Membrane Vesicles ◽  
Cell Polarization ◽  
Cancer Cell Migration ◽  
Signaling Mechanisms ◽  
Complex Signaling ◽  
Dimensional Cell

AbstractMigration is one of the five major behaviors of cells. Although RhoC—a classic member of the Rho gene family—was first identified in 1985, functional RhoC data have only been widely reported in recent years. Cell migration involves highly complex signaling mechanisms, in which RhoC plays an essential role. Cell migration regulated by RhoC—of which the most well-known function is its role in cancer metastasis—has been widely reported in breast, gastric, colon, bladder, prostate, lung, pancreatic, liver, and other cancers. Our review describes the role of RhoC in various types of cell migration. The classic two-dimensional cell migration cycle constitutes cell polarization, adhesion regulation, cell contraction and tail retraction, most of which are modulated by RhoC. In the three-dimensional cell migration model, amoeboid migration is the most classic and well-studied model. Here, RhoC modulates the formation of membrane vesicles by regulating myosin II, thereby affecting the rate and persistence of amoeba-like migration. To the best of our knowledge, this review is the first to describe the role of RhoC in all cell migration processes. We believe that understanding the detail of RhoC-regulated migration processes will help us better comprehend the mechanism of cancer metastasis. This will contribute to the study of anti-metastatic treatment approaches, aiding in the identification of new intervention targets for therapeutic or genetic transformational purposes.

scholarly journals Syndecan-1 facilitates breast cancer metastasis to the brain

2019 ◽  
Author(s):  
Megan R. Sayyad ◽  
Madhavi Puchalapalli ◽  
Natasha G. Vergara ◽  
Sierra Mosticone Wangensteen ◽  
Melvin Moore ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Migration ◽  
Brain Metastasis ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Metastasis ◽  
Breast Cancer Metastasis ◽  
Cancer Cell Migration ◽  
The Brain

AbstractPurposeAlthough survival rates for patients with localized breast cancer have increased, patients with metastatic breast cancer still have poor prognosis. Understanding key factors involved in promoting breast cancer metastasis is imperative for better treatments. In this study, we investigated the role of syndecan-1 (Sdc1) in breast cancer metastasis.MethodsTo assess the role of Sdc1 in breast cancer metastasis, we silenced Sdc1 expression in the triple-negative breast cancer human MDA-MB-231 cell line and overexpressed it in the mouse mammary carcinoma 4T1 cell line. Intracardiac injections were performed in an experimental mouse metastasis model using both cell lines. In vitro transwell blood-brain barrier (BBB) and brain section adhesion assays were utilized to specifically investigate how Sdc1 promotes brain metastasis. A cytokine array was performed to evaluate differences in the breast cancer cell secretome when Sdc1 was silenced.ResultsSilencing expression of Sdc1 in breast cancer cells significantly reduced metastasis to the brain. Conversely, overexpression of Sdc1 increased metastasis to the brain. We found that the reduction in brain metastases with Sdc1 knockdown was likely due to reduced breast cancer cell migration across the BBB and adhesion to the perivascular regions of the brain. However, there was no change in attachment to brain endothelial cells or astrocytes. Loss of Sdc1 also led to changes in breast cancer cell-secreted cytokines, which may influence the BBB.ConclusionsTaken together, our study demonstrates a role for Sdc1 in promoting breast cancer metastasis to the brain. These findings suggest that Sdc1 supports breast cancer cell migration across the BBB through regulation of cytokines, which may modulate the BBB. Further elucidating this mechanism will allow for the development of therapeutic strategies to combat brain metastasis.

scholarly journals CD9 Upregulation-Decreased CCL21 Secretion in Mesenchymal Stem Cells Reduces Cancer Cell Migration

2021 ◽  
Vol 22 (4) ◽  
pp. 1738
Author(s):  
Chia-Chu Hsieh ◽  
Szu-Chun Hsu ◽  
Ming Yao ◽  
Dong-Ming Huang
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Cell Migration ◽  
Cancer Cell ◽  
Cancer Metastasis ◽  
Conditioned Media ◽  
Human Mscs ◽  
Cancer Cell Migration ◽  
Migration Assay

Tetraspanin CD9 is widely expressed on various cell types, such as cancer cells and mesenchymal stem cells (MSCs), and/or cell-released exosomes. It has been reported that exosomal CD9 plays an important role in intercellular communications involved in cancer cell migration and metastasis. However, reports on the effect of the CD9 of MSCs or MSC-derived exosomes on cancer cell migration are still lacking. In this study, using a transwell migration assay, we found that both dextran-coated iron oxide nanoparticles (dex-IO NPs) and ionomycin stimulated exosomal CD9 expression in human MSCs (hMSCs); however, hMSCs could not deliver them to melanoma cells to affect cell migration. Interestingly, a reduced migration of melanoma cell line was observed when the ionomycin-incubated hMSC-conditioned media but not dex-IO NP-labeled hMSC-conditioned media were in the bottom chamber. In addition, we found that dex-IO NPs decreased cellular CD9 expression in hMSCs but ionomycin increased this. Simultaneously, we found that ionomycin suppressed the expression and secretion of the chemokine CCL21 in hMSCs. The silencing of CD9 demonstrated an inhibitory role of cellular CD9 in CCL21 expression in hMSCs, suggesting that ionomycin could upregulate cellular CD9 to decrease CCL21 expression and secretion of hMSCs, which would reduce the migration of B16F10, A549 and U87MG cancer cell lines due to chemoattraction reduction of CCL21. The present study not only highlights the important role of bone marrow-derived hMSCs’ CD9-mediated CCL21 regulation in cancer bone metastasis but also suggests a new distinct pharmaceutical strategy for prevention or/and therapy of cancer metastasis.

scholarly journals 2D protrusion but not motility predicts growth factor–induced cancer cell migration in 3D collagen

2012 ◽  
Vol 197 (6) ◽  
pp. 721-729 ◽  
Author(s):  
Aaron S. Meyer ◽  
Shannon K. Hughes-Alford ◽  
Jennifer E. Kay ◽  
Amalchi Castillo ◽  
Alan Wells ◽  
...  
Keyword(s):  
Cell Migration ◽  
Growth Factor ◽  
Receptor Tyrosine Kinase ◽  
Triple Negative ◽  
Three Dimensional ◽  
Receptor Expression ◽  
Cancer Cell Migration ◽  
Cognate Receptor ◽  
3D Collagen ◽  
High Throughput Experiments

Growth factor–induced migration is a critical step in the dissemination and metastasis of solid tumors. Although differences in properties characterizing cell migration on two-dimensional (2D) substrata versus within three-dimensional (3D) matrices have been noted for particular growth factor stimuli, the 2D approach remains in more common use as an efficient surrogate, especially for high-throughput experiments. We therefore were motivated to investigate which migration properties measured in various 2D assays might be reflective of 3D migratory behavioral responses. We used human triple-negative breast cancer lines stimulated by a panel of receptor tyrosine kinase ligands relevant to mammary carcinoma progression. Whereas 2D migration properties did not correlate well with 3D behavior across multiple growth factors, we found that increased membrane protrusion elicited by growth factor stimulation did relate robustly to enhanced 3D migration properties of the MDA-MB-231 and MDA-MB-157 lines. Interestingly, we observed this to be a more reliable relationship than cognate receptor expression or activation levels across these and two additional mammary tumor lines.

scholarly journals Characterization of three-dimensional cancer cell migration in mixed collagen-Matrigel scaffolds using microfluidics and image analysis

PLoS ONE ◽  
2017 ◽  
Vol 12 (2) ◽  
pp. e0171417 ◽  
Author(s):  
María Anguiano ◽  
Carlos Castilla ◽  
Martin Maška ◽  
Cristina Ederra ◽  
Rafael Peláez ◽  
...  
Keyword(s):  
Image Analysis ◽  
Cell Migration ◽  
Cancer Cell ◽  
Three Dimensional ◽  
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.

The role of aquaporin-5 in cancer cell migration: A potential active participant

2016 ◽  
Vol 79 ◽  
pp. 271-276 ◽  
Author(s):  
Helene H. Jensen ◽  
Frédéric H. Login ◽  
Jennifer S. Koffman ◽  
Tae-Hwan Kwon ◽  
Lene N. Nejsum
Keyword(s):  
Cell Migration ◽  
Cancer Cell ◽  
Cancer Cell Migration ◽  
Aquaporin 5 ◽  
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