scholarly journals Screening of Tumor Suppressor Genes in Metastatic Colorectal Cancer

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Lu Qi ◽  
Yanqing Ding
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Mrna Expression ◽  
Binding Site ◽  
Methylation Level ◽  
Tumor Suppressor Genes ◽  
Enrichment Analysis ◽  
Suppressor Genes ◽  
Genes Expression ◽  
Chromosome 17P13

Most tumor suppressor genes are commonly inactivated in the development of colorectal cancer (CRC). The activation of tumor suppressor genes may be beneficial to suppress the development and metastasis of CRC. This study analyzed genes expression and methylation levels in different stages of CRC. Genes with downregulated mRNA expression and upregulated methylation level in advanced CRC were screened as the potential tumor suppressor genes. After comparing the methylation level of screened genes, we found that MBD1 gene had downregulated mRNA expression and upregulated methylation levels in advanced CRC and continuously upregulated methylation level in the progression of CRC. Enrichment analysis revealed that genes expression in accordance with the elevated expression of MBD1 mainly located on chromosomes 17p13 and 17p12 and 8 tumor suppressor genes located on chromosome 17p13. Further enrichment analysis of transcription factor binding site identified that SP1 binding site had higher enrichment and could bind with MBD1. In conclusion, MBD1 may be a tumor suppressor gene in advanced CRC and affect the development and metastasis of CRC by regulating 8 tumor suppressor genes through binding with SP1.

scholarly journals Patterns of somatic uniparental disomy identify novel tumor suppressor genes in colorectal cancer

2015 ◽  
Vol 36 (10) ◽  
pp. 1103-1110 ◽  
Author(s):  
Keyvan Torabi ◽  
Rosa Miró ◽  
Nora Fernández-Jiménez ◽  
Isabel Quintanilla ◽  
Laia Ramos ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Uniparental Disomy ◽  
Suppressor Genes

Progression of colorectal cancer is associated with multiple tumor suppressor gene defects but inhibition of tumorigenicity is accomplished by correction of any single defect via chromosome transfer

1992 ◽  
Vol 12 (3) ◽  
pp. 1387-1395
Author(s):  
M C Goyette ◽  
K Cho ◽  
C L Fasching ◽  
D B Levy ◽  
K W Kinzler ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Loss Of Function ◽  
Chromosome 18 ◽  
Chromosome 5 ◽  
Suppressor Genes ◽  
Single Defect

Carcinogenesis is a multistage process that has been characterized both by the activation of cellular oncogenes and by the loss of function of tumor suppressor genes. Colorectal cancer has been associated with the activation of ras oncogenes and with the deletion of multiple chromosomal regions including chromosomes 5q, 17p, and 18q. Such chromosome loss is often suggestive of the deletion or loss of function of tumor suppressor genes. The candidate tumor suppressor genes from these regions are, respectively, MCC and/or APC, p53, and DCC. In order to further our understanding of the molecular and genetic mechanisms involved in tumor progression and, thereby, of normal cell growth, it is important to determine whether defects in one or more of these loci contribute functionally in the progression to malignancy in colorectal cancer and whether correction of any of these defects restores normal growth control in vitro and in vivo. To address this question, we have utilized the technique of microcell-mediated chromosome transfer to introduce normal human chromosomes 5, 17, and 18 individually into recipient colorectal cancer cells. Additionally, chromosome 15 was introduced into SW480 cells as an irrelevant control chromosome. While the introduction of chromosome 17 into the tumorigenic colorectal cell line SW480 yielded no viable clones, cell lines were established after the introduction of chromosomes 15, 5, and 18. Hybrids containing chromosome 18 are morphologically similar to the parental line, whereas those containing chromosome 5 are morphologically distinct from the parental cell line, being small, polygonal, and tightly packed. SW480-chromosome 5 hybrids are strongly suppressed for tumorigenicity, while SW480-chromosome 18 hybrids produce slowly growing tumors in some of the animals injected. Hybrids containing the introduced chromosome 18 but was significantly reduced in several of the tumor reconstitute cell lines. Introduction of chromosome 5 had little to no effect on responsiveness, whereas transfer ot chromosome 18 restored responsiveness to some degree. Our findings indicate that while multiple defects in tumor suppressor genes seem to be required for progression to the malignant state in colorectal cancer, correction of only a single defect can have significant effects in vivo and/or in vitro.

scholarly journals Screening of tumor suppressor genes on 1q31.1-32.1 in Chinese patients with sporadic colorectal cancer

2008 ◽  
Vol 121 (24) ◽  
pp. 2479-2486 ◽  
Author(s):  
Chong-zhi ZHOU ◽  
Guo-qiang QIU ◽  
Xiao-liang WANG ◽  
Jun-wei FAN ◽  
Hua-mei TANG ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Chinese Patients ◽  
Sporadic Colorectal Cancer ◽  
Suppressor Genes

scholarly journals The co-regulatory networks of tumor suppressor genes, oncogenes, and miRNAs in colorectal cancer

2017 ◽  
Vol 56 (11) ◽  
pp. 769-787 ◽  
Author(s):  
Martha L. Slattery ◽  
Jennifer S. Herrick ◽  
Lila E. Mullany ◽  
Wade S. Samowitz ◽  
John R. Sevens ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Tumor Suppressor ◽  
Tumor Suppressor Genes ◽  
Regulatory Networks ◽  
Suppressor Genes

scholarly journals An in silico integrative analysis of hepatocellular carcinoma omics databases shows the dual regulatory role of microRNAs either as tumor suppressors or as oncomirs

2021 ◽  
Author(s):  
Mahmoud M. Tolba ◽  
Bangli Soliman ◽  
Abdul Jabbar ◽  
HebaT'Allah Nasser ◽  
Mahmoud Elhefnawi
Keyword(s):  
Tumor Suppressor ◽  
In Silico ◽  
Tumor Suppressor Genes ◽  
Messenger Rna ◽  
Integrative Analysis ◽  
Suppressor Genes ◽  
Short Rnas ◽  
Genes Expression ◽  
Specific Mrnas ◽  
Mirnas Expression

MicroRNAs are well known as short RNAs bases, 22 nucleotides, binding directly to 3'untranslated region (3'UTR) of the messenger RNA to repress their functions. Recently, microRNAs have been widely used as a therapeutic approach for various types of Cancer. MicroRNA is categorized into tumor suppressor and oncomirs. Tumor suppressor microRNAs can repress the pathologically causative oncogenes of the hallmarks of Cancer. However, based on the fact that miRNA has no proper fidelity to bind specific mRNAs due to binding to off-targets, it results in a kind of inverse biological activity. Here, we have executed an in-silico integrative analysis of GEO/TCGA-LIHC of genes/microRNAs expression analysis in HCC, including (446 HCC vs. 146 normal specimens for miRNAs expression ) ad 488 specimens for genes expression. It virtually shows that microRNAs could have an ability to target both oncogenes and tumor suppressor genes that contribute to its dual activity role as a tumor suppressor and oncomirs via miRNA-lncRNA-TFs-PPI Crosstalk. Seven resultant microRNAs show a putative dual role in HCC. It enhances our concluded suggestion of using combination therapy of tumor suppressor genes activators with microRNAs.

Detection and Analysis of RNAs Expression Profile for Methylated Candidate Tumor Suppressor Genes in Nasopharyngeal Carcinoma

2019 ◽  
Vol 19 (6) ◽  
pp. 772-782
Author(s):  
Shuang Zhao ◽  
Ye Zhang ◽  
Xujun Liang ◽  
Maoyu Li ◽  
Fang Peng ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Nasopharyngeal Carcinoma ◽  
Tumor Suppressor ◽  
Promoter Methylation ◽  
Tumor Suppressor Genes ◽  
Enrichment Analysis ◽  
Pathway Enrichment Analysis ◽  
Suppressor Genes ◽  
Multiple Tumor

Background:DNA methylation, which acts as an expression regulator for multiple Tumor Suppressor Genes (TSGs), is believed to play an important role in Nasopharyngeal Carcinoma (NPC) development.Methods:We compared the effects of 5-aza-2-deoxycytidine (decitabine, DAC) on gene expression using RNA sequencing in NPC cells.Results:We analyzed Differentially Expressed Genes (DEGs) in NPC cells using DAC demethylation treatment and found that 2182 genes were significantly upregulated (≥ 2-fold change), suggesting that they may play a key role in cell growth, proliferation, development, and death. For data analysis, we used the Gene Ontology database and pathway enrichment analysis of the DEGs to discover differential patterns of DNA methylation associated with changes in gene expression. Furthermore, we evaluated 74 methylated candidate TSGs from the DEGs in NPC cells and summarized these genes in several important signaling pathways frequently disrupted by promoter methylation in NPC tumorigenesis.Conclusion:Our study analyzes the DEGs and identifies a set of genes whose promoter methylation in NPC cells is reversed by DAC. These genes are potential substrates of DNMT inhibitors and may serve as tumor suppressors in NPC cells.

No Reversal of Demethylation after Azacitidine Treatment in Concordance with Poor Clinical Response.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 4629-4629
Author(s):  
Huong Thi Thanh Tran ◽  
Hee Nam Kim ◽  
JaeSook Ahn ◽  
Il-Kwon Lee ◽  
Deok-Hwan Yang ◽  
...  
Keyword(s):  
Tumor Suppressor ◽  
Clinical Response ◽  
Methylation Level ◽  
Tumor Suppressor Genes ◽  
Gene Mutations ◽  
Molecular Monitoring ◽  
Suppressor Genes ◽  
Promoter Dna Methylation ◽  
History Of ◽  
Promoter Dna

Abstract The epigenetic gene silencing associated with promoter DNA methylation is as powerful as gene mutations in functionally inactivating tumor suppressor genes. Thus, a non-intensive treatment may be changed the natural history of MDS for the first time by the demethylating agent, 5-aza-deoxycytidine (Decitabine) with silenced gene expression by reversal of p15 hypermethylation and protein expression in the bone marrow in MDS. The MS-MLPA (methylation-specific multiplex ligation-dependent probe amplification) ME-001B probemix (MRC-Holland) containing 25 tumor suppressor genes has been used to detect the methylation level in the peripheral blood samples of 29 MDS before azacitidine (Vidaza) and only 6 MDS after 3–5 courses of therapy. Patients that hypermethylated at least 1 gene were 7 of 29, either the common hypermethylating genes as p15, ESR1 or the previously known FHIT in MDS also have occurred. Only two patients except one patient related to either methylation level-reducing gene or removal methylated gene (putative demethylation reversal) have in concordance with clinical response in hematological evidence. Interestingly, three other patients were high methylation level persistently or additional methylated gene after treatment (putative demethylation no reversal or more severe), two patients of these are correspond with no clinical response and one is propensity to progressing leukemia. With IGSF4 gene hypermethylation, to the best of our knowledge, there was no report in MDS. Our results suggest that methylation level possibly contributes to the dignosistic, prognosistic and a molecular monitoring marker after treatment of Azacitidine.

Methylation Profiles of Tumor Suppressor Genes in Inflammatory Bowel Disease-Associated and Sporadic Colorectal Cancer: A Comparison

2011 ◽  
Vol 140 (5) ◽  
pp. S-349
Author(s):  
Marian M. Claessen ◽  
Frank P. Vleggaar ◽  
Marguerite E. Schipper ◽  
John W. Hinrichs ◽  
Remco D. Radersma ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Inflammatory Bowel Disease ◽  
Tumor Suppressor ◽  
Bowel Disease ◽  
Tumor Suppressor Genes ◽  
Sporadic Colorectal Cancer ◽  
Suppressor Genes ◽  
Inflammatory Bowel
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