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Your search keyword '"Ho Kin Chan"' showing total 2 results
Start Over Author "Ho Kin Chan" Topic 030220 oncology & carcinogenesis
2 results on '"Ho Kin Chan"'

1. LTBP-2 confers pleiotropic suppression and promotes dormancy in a growth factor permissive microenvironment in nasopharyngeal carcinoma

Author

Qian Tao, Anne Wing Mui Lee, Josephine Mun Yee Ko, Eric J. Stanbridge, Florence Cheung, Han Chen, Rebecca Kan, Jorma Keski-Oja, Sai Wah Tsao, Eugene R. Zabarovsky, Daniel Chua, Dora L.W. Kwong, Maria Li Lung, Stephen Ho Kin Chan, John M. Nicholls, Pui Man Chiu, Marko Hyytiäinen, and Victor Chun Lam Wong

Subjects
Vascular Endothelial Growth Factor A, Cancer Research, Tumor suppressor gene, Angiogenesis, medicine.medical_treatment, Nasopharyngeal neoplasm, Down-Regulation, Biology, Decitabine, Hydroxamic Acids, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Cell Movement, Cell Line, Tumor, medicine, Tumor Microenvironment, Humans, Promoter Regions, Genetic, 030304 developmental biology, 0303 health sciences, Tumor microenvironment, Nasopharyngeal Carcinoma, Neovascularization, Pathologic, Growth factor, Tumor Suppressor Proteins, Carcinoma, Cell migration, Nasopharyngeal Neoplasms, DNA Methylation, Vascular endothelial growth factor, Gene Expression Regulation, Neoplastic, Vascular endothelial growth factor A, Cell Transformation, Neoplastic, Oncology, chemistry, Latent TGF-beta Binding Proteins, 030220 oncology & carcinogenesis, Cancer research, Azacitidine
Abstract

This study identified LTBP-2 as a pleiotropic tumor suppressor in nasopharyngeal carcinoma, which safeguards against critical malignant behaviors of tumor cells. LTBP-2 expression was significantly decreased or lost in up to 100% of NPC cell lines (7/7) and 80% of biopsies (24/30). Promoter hypermethylation was found to be involved in LTBP-2 silencing. Using a tetracycline-regulated inducible expression system, we unveiled functional roles of LTBP-2 in suppressing colony formation, anchorage-independent growth, cell migration, angiogenesis, VEGF secretion, and tumorigenicity. Three-dimensional culture studies suggested the involvement of LTBP-2 in maintenance of tumor cell dormancy in a growth factor favorable microenvironment.

Published
2012

2. The ECM protein LTBP-2 is a suppressor of esophageal squamous cell carcinoma tumor formation but higher tumor expression associates with poor patient outcome

Author

Han Chen, Johnny Cheuk On Tang, Sai Wah Tsao, Eric J. Stanbridge, Marko Hyytiäinen, Simon Law, Gopesh Srivastava, Qian Tao, Yuen Piu Chan, Maria Li Lung, Kwok Wah Chan, Josephine Mun Yee Ko, Jorma Keski-Oja, and Stephen Ho Kin Chan

Subjects
Cancer Research, Pathology, medicine.medical_specialty, Tumor suppressor gene, Esophageal Neoplasms, Cell, Down-Regulation, Mice, Nude, medicine.disease_cause, 03 medical and health sciences, Mice, 0302 clinical medicine, Nude mouse, Cell Line, Tumor, medicine, Animals, Humans, Genes, Tumor Suppressor, Tumor Stem Cell Assay, 030304 developmental biology, 0303 health sciences, Matrigel, Mice, Inbred BALB C, biology, DNA Methylation, biology.organism_classification, digestive system diseases, Gene expression profiling, medicine.anatomical_structure, Oncology, Latent TGF-beta Binding Proteins, 030220 oncology & carcinogenesis, Microcell-mediated chromosome transfer, Cancer research, Carcinoma, Squamous Cell, Female, Carcinogenesis, Neoplasm Transplantation
Abstract

Our previous studies of chromosome 14 transfer into tumorigenic esophageal squamous cell carcinoma (ESCC) cell line, SLMT, suggested the existence of tumor suppressor genes on chromosome 14. Gene expression profiling of microcell hybrids and the tumor segregants identified an interesting gene, LTBP-2 (latent transforming growth factor β binding protein 2), which has been analyzed here for its role in ESCC. LTBP-2 maps to 14q24 and encodes a secreted protein, which is a component of the extracellular matrix microfibrils. LTBP-2 expression was downregulated in ESCC cell lines and tumor tissues. Promoter hypermethylation was found to be involved in LTBP-2 inactivation. Functional studies indicated its tumor-suppressive roles in ESCC. In the in vitro colony formation and Matrigel three-dimensional culture assays, LTBP-2 decreased the colony-forming abilities of ESCC cell lines. LTBP-2 expression was associated with reduction of cell migrating and invasive abilities. LTBP-2 could also reduce the tube-forming ability of endothelial cells. Moreover, LTBP-2 induced tumor suppression in in vivo nude mouse assays. Tissue microarray immunohistochemical staining analysis indicated that LTBP-2 expression is reduced in tumor tissues when compared to normal tissues, and LTBP-2 expression correlated significantly with the survival of ESCC patients. Thus, LTBP-2 appears to play an important role in ESCC.

Published
2010

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