scholarly journals CDK10 functions as a tumor suppressor gene and regulates survivability of biliary tract cancer cells

2011 ◽  
Vol 27 (4) ◽  
pp. 1266-1276 ◽  
Author(s):  
JIAN-HUA YU ◽  
XIANG-YU ZHONG ◽  
WEI-GUANG ZHANG ◽  
ZHI-DONG WANG ◽  
QIN DONG ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
Biliary Tract ◽  
Biliary Tract Cancer ◽  
Suppressor Gene ◽  
Tract Cancer

scholarly journals Induction of PDCD4 tumor suppressor gene expression by RAR agonists, antiestrogen and HER-2/neu antagonist in breast cancer cells. Evidence for a role in apoptosis

Oncogene ◽  
2004 ◽  
Vol 23 (49) ◽  
pp. 8135-8145 ◽  
Author(s):  
Olubunmi Afonja ◽  
Dominique Juste ◽  
Sharmistha Das ◽  
Sachiko Matsuhashi ◽  
Herbert H Samuels
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
Breast Cancer Cells ◽  
Suppressor Gene ◽  
Her 2

scholarly journals A High-Throughput Screen with Isogenic PTEN+/+ and PTEN−/− Cells Identifies CID1340132 as a Novel Compound That Induces Apoptosis in PTEN and PIK3CA Mutant Human Cancer Cells

2011 ◽  
Vol 16 (4) ◽  
pp. 383-393 ◽  
Author(s):  
Hui-Fang Li ◽  
Adam Keeton ◽  
Michele Vitolo ◽  
Clinton Maddox ◽  
Lynn Rasmussen ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
High Throughput ◽  
Human Cancer ◽  
Genetic Difference ◽  
Suppressor Gene ◽  
Pten Gene ◽  
Target Cells ◽  
Mutant Cells

The PTEN tumor suppressor gene is one of the most commonly mutated genes in human cancer. Because inactivation of PTEN is a somatic event, PTEN mutations represent an important genetic difference between cancer cells and normal cells and therefore a potential anticancer drug target. However, it remains a substantial challenge to identify compounds that target loss-of-function events such as mutations of tumor suppressors. In an effort to identify small molecules that preferentially kill cells with mutations of PTEN, the authors developed and implemented a high-throughput, paired cell-based screen composed of parental HCT116 cells and their PTEN gene-targeted derivatives. From 138 758 compounds tested, two hits were identified, and one, N′-[(1-benzyl-1H-indol-3-yl)methylene]benzenesulfonohydrazide (CID1340132), was further studied using a variety of cell-based models, including HCT116, MCF10A, and HEC1A cells with targeted deletion of either their PTEN or PIK3CA genes. Preferential killing of PTEN and PIK3CA mutant cells was accompanied by DNA damage, inhibition of DNA synthesis, and apoptosis. Taken together, these data validate a cell-based screening approach for identifying lead compounds that target cells with specific tumor suppressor gene mutations and describe a novel compound with preferential killing activity toward PTEN and PIK3CA mutant cells.

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.

scholarly journals Relevance of miR-21 in regulation of tumor suppressor gene PTEN in human cervical cancer cells

BMC Cancer ◽  
2016 ◽  
Vol 16 (1) ◽  
Author(s):  
Oscar Peralta-Zaragoza ◽  
Jessica Deas ◽  
Angélica Meneses-Acosta ◽  
Faustino De la O-Gómez ◽  
Gloria Fernández-Tilapa ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Tumor Suppressor ◽  
Cancer Cells ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Cervical Cancer Cells ◽  
Human Cervical Cancer Cells ◽  
Human Cervical Cancer
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