CCL2 increases MMP-9 expression and cell motility in human chondrosarcoma cells via the Ras/Raf/MEK/ERK/NF-κB signaling pathway

Tang, Chih-Hsin; Tsai, Chia‐Chun

doi:10.1016/j.bcp.2011.11.013

Cited by 101 publications

(107 citation statements)

References 35 publications

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“…Furthermore, a study by Yen et al (30) in which chemotaxis assays were performed in human monocytes was consistent with our result. Moreover, some studies demonstrated that ERK downstream of CCR2B was involved in human chondrosarcoma cell (38), dendritic cell (39), and smooth muscle cell (40) migration, which supported our results. In this study, we clearly demonstrate that both CYTL1 and CCL2 promoted ERK phosphorylation, which is indispensable for its chemotactic activity in human monocytes.…”

Section: Discussionsupporting

confidence: 80%

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Cytokine-like 1 Chemoattracts Monocytes/Macrophages via CCR2

Wang

et al. 2016

The Journal of Immunology

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Cytokine-like 1 (CYTL1) is a novel potential cytokine that was first identified in CD34+ cells derived from bone marrow and cord blood, and it was also found using our immunogenomics strategy. The immunobiological functions of CYTL1 remain largely unknown, and its potential receptor(s) has not been identified. A previous proposed hypothesis suggested that CYTL1 had structural similarities with CCL2 and that CCR2 was a potential receptor of CYTL1. In this study, we verify that CYTL1 possesses chemotactic activity and demonstrate that its functional receptor is CCR2B using a series of experiments performed in HEK293 cells expressing CCR2B or CCR2B-EGFP, including chemotaxis, receptor internalization, and radioactive binding assays. CYTL1 chemoattracts human monocytes but not PBLs, and its chemotactic activity toward monocytes is dependent on the CCR2B-ERK pathway. Furthermore, both human and mouse recombinant CYTL1 protein have chemotactic effects on macrophages from wild-type mice but not from Ccr2−/− mice. Furthermore, the chemotactic activity of CYTL1 is sensitive to pertussis toxin. All of the above data confirm that CCR2B is a functional receptor of CYTL1.

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Section: Discussionsupporting

confidence: 80%

“…Recently, ERK was demonstrated to be a significant player in the CCR2B signal transduction pathway (37,38). In this study, we demonstrated that ERK is responsible for CYTL1 and CCL2-induced chemotaxis in human monocytes.…”

Section: Discussionmentioning

confidence: 55%

Cytokine-like 1 Chemoattracts Monocytes/Macrophages via CCR2

Wang

et al. 2016

The Journal of Immunology

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“…Interestingly, from the coculture of EC and MC versus simultaneously MC alone and EC alone, 17 genes from the 27 known differentially expressed genes were linked to migratory and/or embryonic/cancer stem cell properties: nine overexpressed genes: CCL2, ICAM1, SELE, IL6, TRAF1, SERPINB2, CXCL6, PDGFB and EVX1, and eight underexpressed genes: CFDP1, BLID, RGNEF, MALT1, RANBP9, UPF1, PLAA and ZXDC. More specifically, these genes have demonstrated properties linked to (i) cancer cell migration: CCL2 [26,27], ICAM1 [28], IL6 [29], RGNEF [30] and RANBP9 [31]; (ii) cancer progression and metastasis: CCL2 [26,27,32], ICAM1 [33,34], SELE [35,36], TRAF1 [37], IL6 [29], SERPINB2 [38], CXCL6 [39], BLID [40], MALT1 [41], UPF1 [42], PLAA [43], RGNEF [44], ZXDC [45]; (iii) EMT: CCL2 [46] and IL6 [29] ; and (iv) embryonic and/or cancer stem cell properties: CCL2 [46][47][48] , PDGFB [49] , EVX1 [50], CFDP1 [51] and RANBP9 [52] . Furthermore, the 15 most significantly enriched functional groups analyzed by IPA included: development, cell movement, cancer, and embryonic development.…”

Section: Discussionmentioning

confidence: 99%

Pilot Study on “Pericytic Mimicry” and Potential Embryonic/Stem Cell Properties of Angiotropic Melanoma Cells Interacting with the Abluminal Vascular Surface

Lugassy

Wadehra

et al. 2012

Cancer Microenvironment

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The interaction of tumor cells with the tumor vasculature is mainly studied for its role in tumor angiogenesis and intravascular metastasis of circulating tumor cells. In addition, a specific interaction of tumor cells with the abluminal surfaces of vessels, or angiotropism, may promote the migration of angiotropic tumor cells along the abluminal vascular surfaces in a pericytic location. This process has been termed extravascular migratory metastasis.The abluminal vascular surface may also provide a vascular niche inducing or sustaining stemness to angiotropic tumor cells. This pilot study investigated if angiotropic melanoma cells might represent a subset population with pericytic and embryonic or stem cell properties. Through microarray analysis, we showed that the interaction between melanoma cells and the abluminal surface of endothelial cells triggers significant differential expression of several genes. The most significantly differentially expressed genes have demonstrated properties linked to cancer cell migration (CCL2, ICAM1 and IL6), cancer progression (CCL2, ICAM1, SELE, TRAF1, IL6, SERPINB2 and CXCL6), epithelial to mesenchymal transition (CCL2 and IL6), embryonic/stem cell properties (CCL2, PDGFB, EVX1 and CFDP1) and pericytic recruitment (PDGFB). In addition, bioinformatics-based analysis of the differentially expressed genes has shown that the most significantly enriched functional groups included development, cell movement, cancer, and embryonic development. Finally, the investigation of pericyte/mesenchymal stem cells markers via immunostaining of human melanoma samples revealed expression of PDGFRB, NG2 and CD146 by angiotropic melanoma cells. Taken together, these preliminary data are supportive of the "pericytic mimicry" by angiotropic melanoma cells, and suggest that the interaction between melanoma cells and the abluminal vascular surface induce differential expression of genes linked to cancer migration and embryonic/ stem cell properties.

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“…B-RAF overexpression leads to cell cycle arrest and apoptosis [29]. Mediated by transcription factors AP-1, Ets-1 and NF-κB, RAS/RAF/MEK/ERK signaling induces expression of matrix-degrading proteases, MMP-1, -2, -3, -9 and uPa [30][31][32][33]. RAS (H-, K-, N-RAS) and its downstream effectors enhance tumor cell migration.…”

Section: Influence On the Metastatic Cascadementioning

confidence: 99%

Underlying Mechanisms for Distant Metastasis - Molecular Biology

2017

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Concepts of MetastasisIn 1889, the English surgeon Stephen Paget illustrated his theory on metastasis with the sentence 'When a plant goes to seed, its seeds are carried in all directions, but they can only live and grow if they fall on congenial soil'. He based this 'seed and soil' hypothesis on autopsy records where he detected a discrepancy between the blood supply and frequency of metastasis in specific organs. He concluded that the development of metastasis depends on distinctive features of the tumor cells as well as the specific target organs [1,2]. This concept replaced the mechanistic hypothesis of Rudolf Virchow who considered metastasis as the arrest of tumor cell emboli in the vasculature [2]. Nowadays, metastasis is understood as a complex process of molecular and biochemical events performed by multiple actors. The concept of a 'homogenous seed' has been replaced by a heterogeneous hierarchically organized system of tumorigenic cancer stem cells and their non-tumorigenic progeny [3]. Cancer stem cells are now regarded to be the major driver in metastasis development. In addition, the idea of a sequential development of a cancer from a single primary tumor to the subsequent spread to distant sites was abandoned in the last years and replaced by a model of a simultaneous progression towards metastatic tumor disease. The currently favored model describes the evolution of systemic tumor disease as a parallel development of primary tumor and distant metastasis caused by heterogeneous tumor subpopulations [4].To understand the cellular and molecular basis of metastasis, the most acknowledged approach is the concept of the invasionmetastasis cascade proposed by Isaiah J. Fidler in 2003 and subsequently adapted by Scott Valastyan in 2011 [5,6]. The authors distinguish 6 steps in the process from primary local tumor to distant Keywords Metastasis · Molecular mechanism · Cancer therapy Summary Background:The formation of distant metastases constitutes a complex process with a variety of different genes and pathways involved. To improve patient survival, it is necessary to understand the underlying mechanisms of metastasis to allow for targeted intervention. Methods: This review provides an overview of the general concepts of metastasis, focusing on the most important genes and pathways involved and on interventional strategies. Results: Cancer cells undergo different steps to form metastasis: most prominently, local invasion, intravasation, survival in the circulation, arrest at a distant organ site and extravasation, micrometastasis formation, and metastatic colonization. In order to pass these steps, different molecular pathways are of major importance: EGF/RAS/ RAF/MEK/ERK, PI3K/Akt/mTOR, HGF/Met, Wnt/ -catenin, and VEGF signaling. The HGF/Met regulator MACC1 and the Wnt signaling target S100A4 have been shown to play a major role in the metastatic process. Each gene and pathway provides an opportunity for therapeutic intervention. Conclusion: Since metastasis represents a highly limiting factor in cancer...

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CCL2 increases MMP-9 expression and cell motility in human chondrosarcoma cells via the Ras/Raf/MEK/ERK/NF-κB signaling pathway

Cited by 101 publications

References 35 publications

Cytokine-like 1 Chemoattracts Monocytes/Macrophages via CCR2

Cytokine-like 1 Chemoattracts Monocytes/Macrophages via CCR2

Pilot Study on “Pericytic Mimicry” and Potential Embryonic/Stem Cell Properties of Angiotropic Melanoma Cells Interacting with the Abluminal Vascular Surface

Underlying Mechanisms for Distant Metastasis - Molecular Biology

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