The cancer/testis antigen CAGE induces MMP-2 through the activation of NF-κB and AP-1

Kim, Youngmi; Jeoung, Dooil

doi:10.5483/bmbrep.2009.42.11.758

Cited by 11 publications

(6 citation statements)

References 11 publications

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“…More, ERK1/2 might translocate to the nucleus and activate some transcriptional factor AP-1 to regulate gene transcription [32]. AP-1 locates in the MMP-2 promoter region of MMP-2 gene, thus, ERK1/2 might promote MMP-2 transcription and release [33], [34]. Hence, in order to investigate the role of ERK1/2 in regulating the cell migration and invasion, we successfully determined MMP-2 expression and activity.…”

Section: Discussionmentioning

confidence: 99%

Human Chorionic Gonadotropin β Induces Migration and Invasion via Activating ERK1/2 and MMP-2 in Human Prostate Cancer DU145 Cells

et al. 2013

PLoS ONE

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We previously demonstrated that human chorionic gonadotropin β (hCGβ) induced migration and invasion in human prostate cancer cells. However, the involved molecular mechanisms are unclear. Here, we established a stable prostate cancer cell line overexpressing hCGβ and tested hCGβ-triggered signaling pathways causing cell migration and invasion. ELISA showed that the hCGβ amount secreted into medium increased with culture time after the hCGβ-transfected cells were incubated for 3, 6, 9, 12 and 24 h. More, hCGβ standards promoted MAPK (ERK1/2) phosphorylation and increased MMP-2 expression and activity in both dose- and time-dependent manners in hCGβ non-transfected cells. In addition, hCGβ promoted ERK1/2 phosphorylation and increased MMP-2 expression and activity significantly in hCGβ transfected DU145 cells. Whereas ERK1/2 blocker PD98059 (25 µM) significantly downregulated phosphorylated ERK1/2 and MMP-2. Particularly, hCGβ promoted cell migration and invasion, yet the PD98059 diminished the hCGβ-induced cell motility under those conditions. These results indicated that hCGβ induced cell motility via promoting ERK1/2 phosphorylation and MMP-2 upregulation in human prostate cancer DU145 cells.

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Section: Discussionmentioning

confidence: 99%

Human Chorionic Gonadotropin β Induces Migration and Invasion via Activating ERK1/2 and MMP-2 in Human Prostate Cancer DU145 Cells

et al. 2013

PLoS ONE

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“…Construction and transient transfection of firefly luciferase reporter plasmid were performed as previously described [18]. The sequence of pGL3-MMP-2 promoter construct was confirmed (Sunbio Medical Biotechnology, China).…”

Section: Methodsmentioning

confidence: 99%

POU5F1 Enhances the Invasiveness of Cancer Stem-Like Cells in Lung Adenocarcinoma by Upregulation of MMP-2 Expression

et al. 2013

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Lung cancer is the leading cause of cancer-related human deaths. Exploration of the mechanisms underlying the metastasis of cancer stem-like cells (CSLCs) will open new avenues in lung cancer diagnosis and therapy. Here, we demonstrated that CSLCs-derived from lung adenocarcinoma (LAC) cells displayed highly invasive and migratory capabilities via expressing high levels of POU5F1 and MMP-2. We found that POU5F1 directly regulated MMP-2 transcription via interaction with the promoter of MMP-2. POU5F1 knockdown in LACSLCs reduced MMP-2 protein abundance, leading to inhibition of the cell invasion, migration and tumorigenesis potentials of LAC cells. Clinically, aberrantly high expressions of POU5F1 and MMP-2 were inversely correlated with the survival of LAC patients, and the double-positive POU5F1 and MMP-2 showed the worst prediction for the patient’s poor survival. These results indicate that POU5F1 can bind to the MMP-2 promoter for the degradation of surrounding extracellular matrix, and therefore promote invasive and migratory capabilities of LACSLCs. Moreover, our data implicate that the pathological detection of the double-positive expressions for POU5F1 and MMP-2 will be useful as diagnostic and prognostic biomarkers in LAC to advance anti-metastasis therapy.

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“…To test this hypothesis, we first used a ChIP assay to investigate whether HDAC10 binds to the MMP2 and MMP9 promoter regions. The primers used in the ChIP assay were designed according to the binding site of transcriptional factors in these regions (27)(28)(29)(30)(31)(32)(33)(34). The results indicate that HDAC10 can indeed bind to the promoter regions of MMP2 and MMP9 (Fig.…”

Section: Hdac10 Binds To the Promoter Regions Of Mmp2 And -9 And Deacmentioning

confidence: 99%

Histone Deacetylase (HDAC) 10 Suppresses Cervical Cancer Metastasis through Inhibition of Matrix Metalloproteinase (MMP) 2 and 9 Expression

Song

Zhu

et al. 2013

Journal of Biological Chemistry

113

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Background: Aberrant expression of histone deacetylases (HDACs) has been found in several kinds of cancer. Results: HDAC10, a class IIb HDAC, can suppress cervical cancer metastasis. Conclusion: Unlike most other HDACs, which promote carcinogenesis, HDAC10 serves as a tumor suppressor in cervical cancer. Significance: Isoform-specific HDAC inhibitors could be indicated in the clinical treatment of cervical cancer.

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The cancer/testis antigen CAGE induces MMP-2 through the activation of NF-κB and AP-1

Cited by 11 publications

References 11 publications

Human Chorionic Gonadotropin β Induces Migration and Invasion via Activating ERK1/2 and MMP-2 in Human Prostate Cancer DU145 Cells

Human Chorionic Gonadotropin β Induces Migration and Invasion via Activating ERK1/2 and MMP-2 in Human Prostate Cancer DU145 Cells

POU5F1 Enhances the Invasiveness of Cancer Stem-Like Cells in Lung Adenocarcinoma by Upregulation of MMP-2 Expression

Histone Deacetylase (HDAC) 10 Suppresses Cervical Cancer Metastasis through Inhibition of Matrix Metalloproteinase (MMP) 2 and 9 Expression

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