Matrix metalloproteinase-9 is up-regulated by CCL21/CCR7 interaction via extracellular signal-regulated kinase-1/2 signaling and is involved in CCL21-driven B-cell chronic lymphocytic leukemia cell invasion and migration

Redondo-Muñóz, Javier; Terol, María José; García-Marco, José A.; García-Pardo, Ángeles

doi:10.1182/blood-2007-08-107300

Cited by 88 publications

(79 citation statements)

References 20 publications

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“…These results suggest that the activation of ERK1/2 was involved in CCR7 mediated migration and invasion of BE1 cells. The similar report has been found in B-cell chronic lymphocytic leukemia cell, 26 in which the activation of ERK1/2 signaling pathways is involved in CCL21-driven invasion and migration. But Jun Wang et al 27 have been shown that CCR7 activate phosphoinsitide-3 kinase (PI3K)-mediated invasive pathway in head and neck cancer cells.…”

Section: Discussionsupporting

confidence: 66%

Hypoxia-induced CCR7 expression via HIF-1α and HIF-2α correlates with migration and invasion in lung cancer cells

Qiu²,

Zhang³

et al. 2009

Cancer Biology & Therapy

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Hypoxia, a common phenomenon in human solid tumors, is associated with invasion and metastasis in various tumors. Hypoxia inducible factors (HIFs) are key molecules in the hypoxic response, and regulate the activation of specific genes, which mediate many of the adaptations to hypoxia. CC chemokine receptor 7 (CCR7) has been shown to play a critical role in cell chemotaxis and homing, which are key steps in cancer metastasis. A study has demonstrated that hypoxia could upregulate CCR7 in breast cancer cells. The CCR7 gene presents hypoxia response element (HRE; A / G CGTG). We presumed that hypoxia induced upregulation of HIFs promoted the expression of CCR7 facilitating tumor cells invasion and metastasis. In this study, we firstly examined the relationship of CCR7 and HIF-1α, HIF-2α in 94 cases non-small cell lung cancer (NSCLC) tissues by Immunohistochemistry. The results showed that CCR7 expression correlated positively with HIF-1α and HIF-2α, all of them correlated with clinical stage and lymph node metastasis. Then, we investigated whether hypoxia induce the expression of CCR7 through HIF-1α and/or HIF-2α and observed the effects of upregulated CCR7 on the migration and invasion of lung cancer cells. We found that hypoxia induced HIF-1α and HIF-2α expression, which upregulated CCR7 expression; inhibiting HIF-1α or HIF-2α expression in BE1 and A549 cells by RNAi led to the decrease of CCR7 expression, inhibition of migratory and invasive abilities, and the effects of HIF-1α were more significant. Moreover, the migration and invasion of BE1 cells were increased as well as the expression of p-ERK1/2 after CCR7 transfection, but the cells invasive ability was inhibited after blocking p-ERK1/2 with PD98059 and CCR7 with specific antibody. In summary, our study demonstrated that hypoxia-HIF-1α, 2α-CCR7-ERK1/2 pathway could regulate the migration and invasion of lung cancer cells under hypoxic conditions and promote metastasis of lung cancer.

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Section: Discussionsupporting

confidence: 66%

Hypoxia-induced CCR7 expression via HIF-1α and HIF-2α correlates with migration and invasion in lung cancer cells

Qiu²,

Zhang³

et al. 2009

Cancer Biology & Therapy

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“…However, compared with CXCR4, less is known about the role of CCR7 in regulating the secretion of MMPs. The first research on the relationship between CCR7 and MMPs was performed by Redondo and colleagues [32] . Redondo showed that MMP-9 was regulated by CCL21, the ligand of CCR7, and MMP-9 was involved in B-cell chronic lymphocytic leukemia nodal infiltration.…”

Section: Discussionmentioning

confidence: 99%

Topotecan inhibits cancer cell migration by down-regulation of chemokine CC motif receptor 7 and matrix metalloproteinases

et al. 2009

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Aim:The aim of this study was to investigate the effect of topotecan (TPT) on cancer cell migration. Methods: Growth inhibition of TPT was analyzed by MTT assay, and cancer cell migration was measured by transwell double chamber assay. To verify the effect of TPT on the chemokine receptors CXCR4 and CCR7, quantitative PCR, semiquantitative PCR and Western blot analysis were performed. The secretion of MMP-2 and MMP-9 was detected by enzymelinked immunosorbent assay (ELISA) and gelatin zymography. To evaluate possible contributions of CCR7 to MMP secretion, the overexpression vectors pcDNA3.1 + -CCR7 and CCR7 siRNA were transiently transfected into MDA-MB-435 cells. Results: TPT inhibited cancer cell migration in a dose-dependent manner. Additionally, TPT significantly decreased the expression of CCR7 in both MDA-MB-435 and MDA-MB-231 cells and moderately reduced the expression of CXCR4 in MDA-MB-435 cells. The secretion of MMPs (MMP-2, MMP-9) was also inhibited by TPT. Overexpression of CCR7 increased the secretion of MMP-2/9 and cancer cell migration, whereas knockdown of CCR7 reduced active MMP-2/9 production and migration of MDA-MB-435 cells. Conclusion: TPT inhibited cancer cell migration by down-regulation of CCR7 and MMPs (MMP-2 and MMP-9).

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“…Our data showed that ovarian CD133 þ cells and CD133 À cells have distinct patterns of chemokine and chemokine receptor expression. Several chemokines and chemokine receptors showed much stronger expression in CSLCs than in non-CSLCs; notably, many of these molecules have been reported to play important roles in tumor growth and metastasis in various cancers [42][43][44][45][46]. Previously, several groups have identified CXCR4…”

Section: Discussionmentioning

confidence: 99%

Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133 ⁺ Ovarian Cancer Stem‐Like Cells via NF‐κB‐Mediated MMP‐9 Upregulation

et al. 2012

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The concept of cancer stem cells (CSCs) proposes that solely CSCs are capable of generating tumor metastases. However, how CSCs maintain their invasion and migration abilities, the most important properties of metastatic cells, still remains elusive. Here we used CD133 to mark a specific population from human ovarian cancer cell line and ovarian cancer tissue and determined its hyperactivity in migration and invasion. Therefore, we labeled this population as cancer stem-like cells (CSLCs). In comparison to CD1332 non-CSLCs, chemokine CCL5 and its receptors, CCR1, CCR3, and CCR5, were consistently upregulated in CSLCs, and most importantly, blocking of CCL5, CCR1, or CCR3 effectively inhibits the invasive capacity of CSLCs. Mechanistically, we identified that this enhanced invasiveness is mediated through nuclear factor jB (NF-jB) activation and the consequently elevated MMP9 secretion. Our results suggested that the autocrine activation of CCR1 and CCR3 by CCL5 represents one of major mechanisms underlying the metastatic property of ovarian CSLCs.

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Matrix metalloproteinase-9 is up-regulated by CCL21/CCR7 interaction via extracellular signal-regulated kinase-1/2 signaling and is involved in CCL21-driven B-cell chronic lymphocytic leukemia cell invasion and migration

Abstract: B-cell chronic lymphocytic leukemia (B-CLL

Cited by 88 publications

References 20 publications

Hypoxia-induced CCR7 expression via HIF-1α and HIF-2α correlates with migration and invasion in lung cancer cells

Hypoxia-induced CCR7 expression via HIF-1α and HIF-2α correlates with migration and invasion in lung cancer cells

Topotecan inhibits cancer cell migration by down-regulation of chemokine CC motif receptor 7 and matrix metalloproteinases

Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133 ⁺ Ovarian Cancer Stem‐Like Cells via NF‐κB‐Mediated MMP‐9 Upregulation

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Matrix metalloproteinase-9 is up-regulated by CCL21/CCR7 interaction via extracellular signal-regulated kinase-1/2 signaling and is involved in CCL21-driven B-cell chronic lymphocytic leukemia cell invasion and migration

Abstract: B-cell chronic lymphocytic leukemia (B-CLL

Cited by 88 publications

References 20 publications

Hypoxia-induced CCR7 expression via HIF-1α and HIF-2α correlates with migration and invasion in lung cancer cells

Hypoxia-induced CCR7 expression via HIF-1α and HIF-2α correlates with migration and invasion in lung cancer cells

Topotecan inhibits cancer cell migration by down-regulation of chemokine CC motif receptor 7 and matrix metalloproteinases

Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133 + Ovarian Cancer Stem‐Like Cells via NF‐κB‐Mediated MMP‐9 Upregulation

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Autocrine CCL5 Signaling Promotes Invasion and Migration of CD133 ⁺ Ovarian Cancer Stem‐Like Cells via NF‐κB‐Mediated MMP‐9 Upregulation