Expression of connective tissue growth factor in cartilaginous tumors

Shakunaga, Toshihiko; Ozaki, Toshifumi; Ohara, Nobuya; Asaumi, Koji; Doi, Takeshi; Nishida, Keiichiro; Kawai, Akira; Nakanishi, Tohru; Takigawa, Masaharu; Inoue, Hajime

doi:10.1002/1097-0142(20001001)89:7<1466::aid-cncr8>3.0.co;2-g

Cited by 92 publications

(49 citation statements)

References 30 publications

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“…High level of CTGF expression positively correlated with bone metastasis of breast cancer [29], progression of cervical tumors [30], esophageal carcinoma [31] and Wilms' tumor [32], poor prognosis of esophageal adenocancinoma, glioblastoma [33], breast cancer, gastric cancer [34], aggressive behavior and invasiveness of pancreatic cancer cells [35]. Conversely, CTGF expression is negatively correlated with the proliferation activity and tumor grade of chondrosarcoma [36] and non-small-cell lung cancer [37]. These disparities might result from the diversity of CTGF structure, expression level, and binding partners in different tumor types, necessitating the development of more refined detection measures which can differentiate the existence of the different modules and their combinations.…”

Section: Discussionmentioning

confidence: 99%

In vitro selection and characterization of deoxyribonucleic acid aptamers against connective tissue growth factor

Huo

Tian

et al. 2015

Biochemical and Biophysical Research Communications

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Section: Discussionmentioning

confidence: 99%

In vitro selection and characterization of deoxyribonucleic acid aptamers against connective tissue growth factor

Huo

Tian

et al. 2015

Biochemical and Biophysical Research Communications

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“…At the same time, this particular heparan sulfate-rich setting may be related to the pronounced expression level for VEGF 189 , which has higher binding affinity for heparan sulfates. In addition to heparan sulfate proteoglycans, the myxochondroid stroma has been shown to be rich in connective tissue growth factor (CTGF) [13,30] and chondromodulin-I [17], which are also regarded as angiogenic inhibitors.…”

Section: Discussionmentioning

confidence: 99%

Vascular endothelial growth factor in salivary pleomorphic adenomas: one of the reasons for their poorly vascularized stroma

et al. 2005

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To better understand the poorly vascularized background of the stroma of pleomorphic adenomas, we attempted to determine the expression of molecules related to blood vessels and hypoxic conditions in pleomorphic adenoma. Surgical specimens and tumor cells in primary culture of salivary pleomorphic adenomas were used for immunohistochemistry for CD31, vascular endothelial growth factor (VEGF) and its receptors Flk-1 and Flt-1, as well as for hypoxia markers, such as hypoxia-inducible factor-1alpha (HIF-1alpha) and lactate dehydrogenase-1 (LDH). At the same time, alternative splicing modes of the VEGF gene and expression levels of the HIF-1alpha gene were analyzed in surgical specimens by means of reverse-transcription polymerase chain reaction (RT-PCR) and direct sequencing of the PCR products. In addition to co-immunolocalization with CD31+ vascular endothelial cells, VEGF and its receptors were demonstrated in normal duct epithelial and myoepithelial cells as well as in tumor cells in ductal structures and in myxochondroid stromata. Immunolocalizations for HIF-1alpha and LDH were confirmed in the VEGF-positive area. Immunofluorescence signals for VEGF and others were confirmed in pleomorphic adenoma cells in culture. RT-PCR results showed that there were at least four splicing modes of the VEGF gene, among which VEGF(121) was most enhanced, and higher HIF-1alpha levels in pleomorphic adenomas. The results suggest that pleomorphic adenoma cells produce VEGF in several functional forms for their own proliferation or differentiation, and that the VEGF expression is controlled by hypoxic circumstances of poorly vascularized pleomorphic adenomas.

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“…In contrast to that, downregulation of CTGF was found in lung cancer [16] and colon cancer [17], in which forced expression of CTGF blocked invasion and metastasis of the cancer cells both in vitro and in vivo. Also, CTGF expression level correlates with increased survival in chondrosarcoma patients [18]. These disparities in expression in different type of tumors imply that the function of CTGF may be cell type specific.…”

Section: Introductionmentioning

confidence: 99%

CTGF is overexpressed in papillary thyroid carcinoma and promotes the growth of papillary thyroid cancer cells

et al. 2011

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Connective tissue growth factor (CTGF or CCN2), which belongs to the CCN family, is a secreted protein. It has been implicated in various biological processes, such as cell proliferation, migration, angiogenesis, and tumorigenesis. In this study, we found that CTGF expression level was elevated in primary papillary thyroid carcinoma (PTC) samples and correlated with clinical features, such as metastasis, tumor size, and clinical stage. Overexpression of CTGF in PTC cells accelerated their growth in liquid culture and soft agar as well as protecting PTC cells from apoptosis induced by IFN-gamma treatment. Downregulation of CTGF in PTC cells inhibits cell growth in liquid culture and soft agar and induces the activation of caspase pathway and sensitized PTC cells to apoptosis. Our data suggest that CTGF plays an important role in PTC progression by supporting tumor cell survival and drug resistance, and CTGF may be used as a potential tumor marker for PTC diagnosis.

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Expression of connective tissue growth factor in cartilaginous tumors

Cited by 92 publications

References 30 publications

In vitro selection and characterization of deoxyribonucleic acid aptamers against connective tissue growth factor

In vitro selection and characterization of deoxyribonucleic acid aptamers against connective tissue growth factor

Vascular endothelial growth factor in salivary pleomorphic adenomas: one of the reasons for their poorly vascularized stroma

CTGF is overexpressed in papillary thyroid carcinoma and promotes the growth of papillary thyroid cancer cells

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