scholarly journals Tumor suppressor gene NGX6 induces changes in protein expression profiles in colon cancer HT-29 cells

2012 ◽  
Vol 44 (7) ◽  
pp. 584-590 ◽  
Author(s):  
Y. Li ◽  
Y. Luo ◽  
X. Wang ◽  
S. Shen ◽  
H. Yu ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Tumor Suppressor ◽  
Protein Expression ◽  
Tumor Suppressor Gene ◽  
Expression Profiles ◽  
Suppressor Gene ◽  
Protein Expression Profiles ◽  
Ht 29

scholarly journals The tumor suppressor gene RhoBTB1 is a novel target of miR-31 in human colon cancer

2012 ◽  
Vol 42 (2) ◽  
pp. 676-682 ◽  
Author(s):  
RUI-SI XU ◽  
XIAO-DONG WU ◽  
SI-QI ZHANG ◽  
CHANG-FENG LI ◽  
LEI YANG ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Human Colon ◽  
Suppressor Gene ◽  
Human Colon Cancer ◽  
Novel Target

The NBL1 tumor suppressor gene is downregulated in colon cancer by promoter methylation

2004 ◽  
Vol 199 (3) ◽  
pp. 92 ◽  
Author(s):  
Jimmy C. Sung ◽  
Susan McCarthy ◽  
Joel Turner ◽  
C.G. Li ◽  
Timothy J. Yeatman
Keyword(s):  
Colon Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Promoter Methylation ◽  
Suppressor Gene

NTRK3 as a novel tumor suppressor gene in colorectal cancer.

2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 469-469
Author(s):  
Yanxin Luo ◽  
Andrew Kaz ◽  
Samornmas Kanngurn ◽  
William M. Grady
Keyword(s):  
Colorectal Cancer ◽  
Colon Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Aberrant Methylation ◽  
Colon Cancer Cells ◽  
Colon Adenomas ◽  
Colon Cancer Cell Lines

469 Background: Neurotrophin tyrosine kinase receptor 3 (NTRK3) is a receptor tyrosine kinase that has been shown to be an oncogene in breast cancer and possibly in hepatocellular carcinoma. NTRK3 is a trophic dependence receptor, which is a recently described class of receptors that initiate signaling in both the ligand bound and unbound states. Through a genome-wide screen for aberrantly methylated genes, we identified aberrantly methylated NTRK3 as a frequently methylated gene in colon cancer. The aim for the present study is to determine if NTRK3 is an epigenetically silenced tumor suppressor gene in colorectal cancer. Methods: NTRK3 promoter methylation was analyzed in human colon cancer cell lines, normal colon epithelium tissue, colorectal adenomas and colorectal cancers using quantitative methylation-specific PCR and bisulfite sequencing. NTRK3 mRNA and protein expression were studied using quantitative real-time PCR, immunohistochemistry and western blotting respectively. The tumor suppressor function of NTRK3 was examined by assessing the effect of NTRK3 on cell apoptosis, cell migration and in vitro colony formation assays in colon cancer cell lines stably transfected with an NTRK3 expression construct in the presence or absence of NT-3. Results: NTRK3 is methylated in 60% of colon adenomas and in 57% of colorectal cancers. The aberrant methylation of NTRK3 suppresses NTRK3 expression and releases colon cancer cells from NTRK3 mediated apoptosis induced by the expression of NTRK3 in the absence of the ligand NT-3 via the activation of MAPK/ERK pathway. Methylation of NTRK3 also releases colon cancer cells from NTRK3 mediated suppression of motility and anchorage independent growth. The addition of NT3 to colon cancer cells transfected with NTRK3 inhibits the tumor suppressor effects of NTRK3. Conclusions: The aberrant methylation of NTRK3 is likely functionally relevant for colorectal cancer formation as NTRK3 appears to be a conditional tumor suppressor gene in the colon depending on the expression status of its ligand NT-3. NTRK3 is a novel aberrantly methylated conditional tumor suppressor gene that is frequently methylated in colon adenomas and cancers and whose discovery reveals possible novel treatment approaches to colon cancer.

Analysis of p53 Tumor Suppressor Gene, H-ras Protooncogene and Proliferating Cell Nuclear Antigen (PCNA) in Squamous Cell Carcinomas of HRA/Skh Mice Following Exposure to 8-Methoxypsoralen (8-MOP) and UVA Radiation (PUVA Therapy)

2005 ◽  
Vol 33 (2) ◽  
pp. 292-299 ◽  
Author(s):  
Luca Lambertini ◽  
Kezia Surin ◽  
Thai-Vu T. Ton ◽  
Natasha Clayton ◽  
June K. Dunnick ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Protein Expression ◽  
Tumor Suppressor Gene ◽  
Squamous Cell ◽  
Suppressor Gene ◽  
Squamous Cell Carcinomas ◽  
Puva Therapy ◽  
P53 Tumor Suppressor ◽  
Ras Genes ◽  
P53 Tumor Suppressor Gene

Treatment with 8-methoxypsoralen (8-MOP) and ultraviolet radiation (primarily UVA), called PUVA therapy, has been used to treat different chronic skin diseases but led to a significant increased risk for skin cancer. The National Toxicology Program (NTP) performed a study in mice treated with PUVA that showed a significant increase in squamous cell carcinomas of the skin. In the present study, we evaluated the protein expression of p53 and PCNA and DNA mutations of p53 and H-ras genes in both hyperplastic and neoplastic squamous cell lesions from the NTP study. By immunohistochemical staining, protein expression of both p53 and PCNA was detected in 3/16 (19%) of hyperplastic lesions and 14/17 (82%) of SCCs in groups treated with both 8-MOP and UVA. The mutation frequency of p53 in SCCs from mice administered 8-MOP plus UVA was 15/17 (88%) with a predominant distribution of mutations in exon 6 (14/15 – 93%). No H-ras mutations were detected in the hyperplastic lesions/tumors. The mutagenic effect of PUVA on the p53 tumor suppressor gene may lead to a conformational modification and inactivation of the p53 protein, which are considered critical steps in PUVA-induced skin carcinogenesis. The p53 mutational frequency and patterns from our study were different from those reported in human PUVA-type tumors.

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