CDH12 promotes the invasion of salivary adenoid cystic carcinoma

Wang, Jin-Feng; She, Lin; Su, Bogong; Ding, Lin‐Can; Zheng, Fei-Fei; Zheng, Duo

doi:10.3892/or.2011.1286

Cited by 12 publications

(18 citation statements)

References 19 publications

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“…CDH12 can promote the migration and invasion ability of salivary adenoid cystic carcinoma [11]. According to our findings, CDH12 may be an oncogene and promote the malignant progression of CRC cells.…”

Section: Discussionmentioning

confidence: 56%

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Cadherin-12 contributes to tumorigenicity in colorectal cancer by promoting migration, invasion, adhersion and angiogenesis

Zhao

Feng

et al. 2013

J Transl Med

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BackgroundCadherin 12 (CDH12), which encodes a type II classical cadherin from the cadherin superfamily, may mediate calcium-dependent cell adhesion. It has been demonstrated that CDH12 could play an important role in the invasion and metastasis of salivary adenoid cystic carcinoma. We decided to investigate the relationship between CDH12 expression level and clinicopathologic variables in colorectal carcinoma (CRC) patients and to explore the functions of CDH12 in tumorigenesis in CRC.MethodsThe expression levels of CDH12 in colorectal carcinoma tissues were detected by immunohistochemistry. Real-time PCR and Western Blot were used to screen CDH12 high-expression cell lines. CCK-8 assay was used to detect the proliferation ability of CRC cells being transfected by shRNAs against CDH12. The wound assay and transwell assay were performed to test migration and invasion ability. The importance of CDH12 in cell-cell junctions was detected by cell adhesion assay and cell aggregation assay. Endothelial tube formation assay was used to test the influence of CDH12 on angiogenesis.ResultsStatistical analysis of clinical cases revealed that the positive rate of CDH12 was higher in the CRC tumor tissues compared with the adjacent non-tumor tissues. The expression levels of CDH12 in CRC patients are significantly correlated with invasion depth. Consistently, the ability of proliferation, migration and invasion were suppressed when CDH12 was decreased in CRC cells transfected with shRNAs. Cell adhesion assay and cell aggregation assay presented that tumor cells tend to disperse with the lack of CDH12. Endothelial tube formation assay showed that down-regulation of CDH12 could obviously inhibit the process of angiogenesis, implying that CDH12 may play an important role in tumor metastasisConclusionOur results showed that CDH12 promotes proliferation, migration, invasion, adhesion and angiogenesis, suggesting that CDH12 may be an oncogene in colorectal cancer. CDH12 is expected to become a new diagnostic and prognostic marker and a novel target of the treatment of colorectal cancer.

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Section: Discussionmentioning

confidence: 56%

“…This indicates that CDH12 acts as a tumor suppressor gene in the non-small-cell lung cancer [10]. In addition, CDH12 is able to promote the migration and invasion ability of salivary adenoid cystic carcinoma [11]. However, the function of CDH12 in colorectal cancer is unclear.…”

Section: Introductionmentioning

confidence: 99%

Cadherin-12 contributes to tumorigenicity in colorectal cancer by promoting migration, invasion, adhersion and angiogenesis

Zhao

Feng

et al. 2013

J Transl Med

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“…Nevertheless, mQTL genes were also enriched in other cancer-related pathways. For example, five mQTL putative genes are part of the cadherin family, and at least two ( CHD12 and CHD13 ) have been broadly studied for their role in cancer (72–74). Genes related to angiogenesis and vascular permeability pathways had also significant matches, and at least one of them ( NRP1 ) has been studied before in meningioma (49).…”

Section: Discussionmentioning

confidence: 99%

An Integrative Analysis of Meningioma Tumors Reveals the Determinant Genes and Pathways of Malignant Transformation

Gómez¹,

Orgueira

2014

Front. Oncol.

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Meningiomas are frequent central nervous system neoplasms, which despite their predominant benignity, show sporadically malignant behavior. Type 2 neurofibromatosis and polymorphisms in several genes have been associated with meningioma risk and are probably involved in its pathogenesis. Although GWAS studies have found loci related to meningioma risk, little is known about the factors determining malignant transformation. Thus, this study is aimed to identify the genomic and transcriptomic factors influencing evolution from benignity toward aggressive phenotypes. By applying an integrative bioinformatics pipeline combining public information on a wealth of biological layers of complexity (from genetic polymorphisms to protein interactions), this study identified a module of co-expressed genes highly correlated with tumor stage and statistically linked to several genomic regions (module Quantitative Trait Loci, mQTLs). Ontology analysis of the transcription hub genes identified microtubule-associated cell-cycle processes as key drivers of such network. mQTLs and single nucleotide polymorphisms associated with meningioma stage were replicated in an alternative meningioma cohort, and integration of these results with up-to-date scientific literature and several databases retrieved a list of genes and pathways with a potentially important role in meningioma malignancy. As a result, cytoskeleton and cell–cell adhesion pathways, calcium-channels and glutamate receptors, as well as oxidoreductase and endoplasmic reticulum-associated degradation pathways were found to be the most important and redundant findings associated to meningioma progression. This study presents an integrated view of the pathways involved in meningioma malignant conversion and paves the way for the development of new research lines that will improve our understanding of meningioma biology.

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“…Zhang et al reported that expression levels of E-cadherin-catenin are positively correlated with the degree of SACC cell differentiation [13]. Wang JF et al found that N-cadherin was abnormally expressed in highly metastatic SACC tissue, promoting invasion and migration in SACC cells [14]. Although evidence on the relationship between cadherin family genes and SACC is increasing, the role of the cadherin-4 gene (CDH4) in SACC remains unknown.…”

Section: Introductionmentioning

confidence: 99%

CDH4 suppresses the progression of salivary adenoid cystic carcinoma via E-cadherin co-expression

et al. 2016

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The cadherin-4 gene (CDH4) of the cadherin family encodes non-epithelial R-cadherin (R-cad); however, the function of this gene in different types of cancer remains controversial. In this study, we found higher expression of CDH4 mRNA in a salivary adenoid cystic carcinoma (SACC) cell line with low metastatic potential (SACC-83) than in a cell line with high metastatic potential (SACC-LM). By analyzing 67 samples of SACC tissues and 40 samples of paraneoplastic normal tissues, we found R-cad highly expressed in 100% of normal paraneoplastic tissue but only expressed in 64% of SACC tumor tissues (P<0.001). Knockdown of CDH4 expression in vitro promoted the growth, mobility and invasion of SACC cells, and in vivo experiments showed that decreased CDH4 expression enhanced SACC tumorigenicity. Furthermore, CDH4 suppression resulted in down-regulation of E-cadherin (E-cad), which is encoded by CDH1 gene and is a well-known tumor suppressor gene by inhibition of cell proliferation and migration. These results indicate that CDH4 may play a negative role in the growth and metastasis of SACC via co-expression with E-cadherin.

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CDH12 promotes the invasion of salivary adenoid cystic carcinoma

Cited by 12 publications

References 19 publications

Cadherin-12 contributes to tumorigenicity in colorectal cancer by promoting migration, invasion, adhersion and angiogenesis

Cadherin-12 contributes to tumorigenicity in colorectal cancer by promoting migration, invasion, adhersion and angiogenesis

An Integrative Analysis of Meningioma Tumors Reveals the Determinant Genes and Pathways of Malignant Transformation

CDH4 suppresses the progression of salivary adenoid cystic carcinoma via E-cadherin co-expression

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