CCL20/CCR6 promotes the invasion and migration of thyroid cancer cells via NF-kappa B signaling-induced MMP-3 production

Zeng, Wei; Chang, Hao; Ma, Min; Li, Yanwei

doi:10.1016/j.yexmp.2014.06.012

Cited by 51 publications

(38 citation statements)

References 26 publications

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“…In addition, survival analysis indicated that either C23 or BMPRII expression serves as an independent prognostic factor in gastric cancer patients. In accordance with our results, published articles identified that the chemical receptor C23 and BMPRII highly expressed in many tumors, such as thyroid cancer [16], hepatocellular carcinoma [17], and also closely associated with metastasis and poor prognosis. Considering all things, we assumed that C23-BMP2 pathway was implicated in the progression of gastric cancer.…”

Section: Discussionsupporting

confidence: 92%

C23 protein meditates bone morphogenetic protein-2-mediated EMT via up-regulation of Erk1/2 and Akt in gastric cancer

2015

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In our previous study, the epithelial-to-mesenchymal transition (EMT) has been identified to be involved in gastric cancer progression. Notably, nuclear protein C23 and bone morphogenetic protein-2 (BMP2) have been linked into EMT. However, the specific mechanisms underlying BMP2 pathway-mediated EMT are not still unraveled. In this study, we adopted immunohistochemistry and immunoblotting to determine the expression of C23 and BMP2 receptor II (BMPR-II) in 90 gastric cancer samples and cell lines. Subsequently, relevant cell lines were selected to be treated with si-C23 or si-BMPRII and the detection of in vitro assay. Our results revealed that both C23 and BMPRII were aberrantly and constitutively expressed in gastric cancer specimens and cell lines, whose expression was positively associated with metastasis, stage and differentiation, and portended poor survival outcome of gastric cancer patients. In vitro assay validated the increased expression of p-Erk1/2, p-Akt, vimentin, N-cadherin, and MMP2 in BMP2-stimulated MGC803 cells, which was in a dose-dependent manner. By contrast, si-C23 treatment attenuated the BMP2-stimulated expression of p-Erk1/2, p-Akt, vimentin, N-cadherin, and MMP2. Also, the treatment of either si-C23 or si-BMPRII decreased the ability of migration and invasion of MGC803 cells. In conclusion, C23 mediates BMP2-induced EMT progression via the up-regulation of Erk1/2 and Akt signaling pathway in gastric cancer, which indicated both C23 and BMPRII pathway could be recommended as prospective targets or biomarkers to antagonize the progression of gastric cancer.

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Section: Discussionsupporting

confidence: 92%

C23 protein meditates bone morphogenetic protein-2-mediated EMT via up-regulation of Erk1/2 and Akt in gastric cancer

2015

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“…49 Also CCL20 was found to promote TC cell invasion and migration in vitro, presumably due to the activation of NF-kB-dependent upregulation of MMP-3. 50 We have recently found that the oncolytic adenovirus dl922-947 reduced CXCL8/IL-8 and CCL2 production by ATC cell lines. 51 Interestingly, dl922-947 treatment impaired ATCinduced angiogenesis and favored the switch of tumor macrophages toward an M1 phenotype.…”

Section: Chemokinesmentioning

confidence: 96%

The immune network in thyroid cancer

2016

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The immune system plays critical roles in tumor prevention, but also in its initiation and progression. Tumors are subjected to immunosurveillance, but cancer cells generate an immunosuppressive microenvironment that favors their escape from immune-mediated elimination. During chronic inflammation, immune cells can contribute to the formation and progression of tumors by producing mitogenic, prosurvival, proangiogenic and lymphangiogenic factors. Thyroid cancer is the most frequent type of endocrine neoplasia and is the most rapidly increasing cancer in the US. In this review, we discuss recent findings on how different immune cells and mediators can contribute to thyroid cancer development and progression.

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“…According to our raw data, the expression of CCL20-induced p-ERK, p-AKT, MMP2, MMP9 and ICAM-1 protein was affected by the si-nucleolin or si-CCR6 treatment. Recent reports identified that ERK and AKT pathway regulates the expression and release of MMPs family, and affected the synthesis of ICAM-1 protein [18][19][20]. These results indicated that nucleolin participated in the initiation and activation of CCL20-induced ERK and AKT pathways, leading to the increased expression of MMP2, MMP9 and ICAM-1 protein.…”

Section: Discussionmentioning

confidence: 81%

The involvement of cell surface nucleolin in the initiation of CCR6 signaling in human hepatocellular carcinoma

et al. 2015

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In recent years, the chemokine CC receptor 6 (CCR6) and its ligand CCL20 were reported to play an essential role in hepatocellular carcinoma (HCC). However, the role of cell surface nucleolin in the CCR6 pathway of HCC is not well featured. Using immunohistochemistry, Western blotting, siRNA, wound healing and transwell assay, we investigated the relationships of cell surface nucleolin and CCR6 signaling in HCC. In the present study, our findings identified that cell surface nucleolin and CCR6 protein were stained in most of HCC tissues (64, 68 %, respectively) and differently expressed in HCC cell lines; meanwhile, both expression has an association with advanced stage, lymph node metastasis and poor 5-year prognosis. According to in vitro assays, we found that the silencing of either cell surface nucleolin or CCR6 inhibited the protein expression of p-ERK, p-AKT, MMP2, MMP9 and ICAM-1 in the CCL20-stimulated HCCLM6 cells. Functional analysis revealed that cell surface nucleolin or CCR6 silencing significantly hampered HCCLM6 cell motility and invasiveness ability, when compared with control. In conclusion, this work suggests that cell surface nucleolin participates in the initiation of CCR6 pathway and biological behaviors of HCC, leading to HCC cell adhesion, migration and invasive behavior. In the clinical practice, cell surface nucleolin and CCR6 are recommended to predict poor prognosis and be used as a useful target for HCC patients.

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CCL20/CCR6 promotes the invasion and migration of thyroid cancer cells via NF-kappa B signaling-induced MMP-3 production

Cited by 51 publications

References 26 publications

C23 protein meditates bone morphogenetic protein-2-mediated EMT via up-regulation of Erk1/2 and Akt in gastric cancer

C23 protein meditates bone morphogenetic protein-2-mediated EMT via up-regulation of Erk1/2 and Akt in gastric cancer

The immune network in thyroid cancer

The involvement of cell surface nucleolin in the initiation of CCR6 signaling in human hepatocellular carcinoma

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