Interrelationship between chromosome 8 aneuploidy,<i>C-MYC</i>amplification and increased expression in individuals from northern Brazil with gastric adenocarcinoma

Calcagno, Danielle Queiroz

doi:10.3748/wjg.v12.i38.6207

Cited by 77 publications

(92 citation statements)

References 36 publications

(31 reference statements)

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“…We have also previously seen MYC amplification in intestinal adenocarcinoma by dual-color fluorescence in situ hybridization (FISH), such as homogeneously staining chromosomal regions and double minutes, supporting our CGH results [56] . Our findings support that these two histological GC types follow different genetic pathways.…”

Section: Mechanisms Of Myc Deregulation In Gastric Cancersupporting

confidence: 88%

“…Yamashita et al [74] identified chromosomal translocations involved in 8q24 breakpoint by spectral karyotyping (SKY) analysis of established GC cell lines and cancerous ascitic fluids. In a previous study, our findings suggested that translocations can be related to diffusetype GC using FISH assay [37,56] . Epigenetic events play a significant role in cancer development and progression.…”

mentioning

confidence: 53%

“…We found that MYC protein was expressed in all cases of both intestinal-and diffuse-type gastric adenocarcinoma samples of individuals from Northern Brazil [37] . Table 1 [ shows the proportion of cases with MYC aberration in several GC studies.…”

Section: Myc and Gastric Carcinogenesismentioning

confidence: 77%

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MYC and gastric adenocarcinoma carcinogenesis

Calcagno¹,

Leal²,

Assumpção³

et al. 2008

WJG

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MYC is an oncogene involved in cell cycle regulation, cell growth arrest, cell adhesion, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function. It has been described as a key element of several carcinogenesis processes in humans. Many studies have shown an association between MYC deregulation and gastric cancer. MYC deregulation is also seen in gastric preneoplastic lesions and thus it may have a role in early gastric carcinogenesis. Several studies have suggested that amplification is the main mechanism of MYC deregulation in gastric cancer.In the present review, we focus on the deregulation of the MYC oncogene in gastric adenocarcinoma c a r c i n o g e n e s i s , i n c l u d i n g i t s a s s o c i a t i o n w i t h Helicobacter pylori (H pylori ) MYC AND CANCERMYC gene was found to be the cellular homolog of retroviral v-myc oncogene about 30 years ago [12][13][14] . It is located on chromosomal region 8q24.1, has 3 exons [15,16] and encodes a nuclear phosphoprotein [17] . MYC has to heteromerize with MAX, a protein expressed constitutively, to acquire DNA-binding activity. MYC/MAX dimmers are made viable by a basic region helix-loop-helix leucine-zipper motif (bHLHZip), conserved sequences in the carboxyl terminus of both proteins. MYC/MAX dimmers bind to E-box sequence CACGTG in the promoters of specific target genes and stimulate their transcription [18] . MYC has an effect on up to about 15% of genes in genomes of many organisms, from flies to humans [19] . Groups of genes involved in cell cycle regulation, metabolism, ribosome biogenesis, protein synthesis, and mitochondrial function are over-represented in the Myc target gene network.MYC also consistently represses genes involved in cell growth arrest and cell adhesion [20] . Dominguez-Sola et al [21] recently showed that Myc interacts with the prereplicative complex and localizes to early sites of DNA synthesis. Thus, it also has a direct role in the control of DNA replication.MYC regulates transcription from its targets through several mechanisms, including recruitment of histone acetylases, chromatin modulating proteins, basal transcription factors and DNA methyltransferase [22][23][24][25][26] . Protein products of MYC target genes g o on to mediate the downstream effects of MYC on cell biology. MYC is then rapidly degraded, and the pathway switches to a transcriptionally repressive state when MAX dimerizes with a group of related bHLH-Zip proteins, the MAD family, that act as MYC antagonists [27] ( Figure 1).MYC expression might be regulated transcriptionally (initiation and elongation), post-transcriptionally (mRNA stability and translation) or post-translationally (protein stability) [28] . MYC is generally recognized as an important regulator of proliferation, growth, differentiation and apoptosis [29,30] . Therefore, it is also accepted that the deregulation of MYC expression is a major event in cancer pathogenesis or progression. Deregulated expression of a wild-type MYC protein is suff...

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Section: Mechanisms Of Myc Deregulation In Gastric Cancersupporting

confidence: 88%

mentioning

confidence: 53%

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MYC and gastric adenocarcinoma carcinogenesis

Calcagno¹,

Leal²,

Assumpção³

et al. 2008

WJG

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“…The membrane undersurface was coated with 200 µl FCS for 1 h at 37˚C and blocked with 200 µl migration buffer (0.5% BSA in DMEM) for 30 min at 37˚C. The lower chamber was filled with 500 µl of migration buffer, following which cells were plated in the upper chamber of 4 wells/treatment at a density of 1x10 5 in 100 µl of migration buffer and incubated at 37˚C for 4 h. Following incubation, cells in the upper compartment were trypsinized and counted by the CASY 1 counter (Sharfe System, Reutingen, Germany). Cells that had migrated to the lower surface of the filter were also trypsinized and counted.…”

Section: Analysis Of Transfectants Rt-pcr and Western Blot Analysismentioning

confidence: 99%

The role of calcyclin gene in the proliferation and migration of gastric cancer cells

Zhang

Hou²,

Kai³

et al. 2011

Oncol Rep

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Abstract. The aim of this study was to investigate the influence of calcyclin on the growth, proliferation, apoptosis, invasion and cell cycle of gastric cancer cell lines in order to elucidate the role that calcyclin plays in gastric adenocarcinoma. Calcyclin cDNA was subcloned into a constitutive vector pcDNA3.1 followed by liposome-mediated transfection in the MKN45 gastric cancer cell line. Stable transfectants were selected and appraised. Specific inhibition of calcyclin was achieved using a vector-based siRNA system by transfection into the SGC7901 gastric cancer cell line. The apoptosis and cell cycle of these clones were analyzed by flow cytometry. Growth and proliferation were analyzed by cell growth curves and a colonyformation assay, respectively. The invasion of these clones was analyzed by a cell migration assay. MKN-calcyclin grew faster compared to MKN45 and MKN-PC (MKN45 transfected with pcDNA3.1 vector). SGC-SR1,2 grew slower compared to SGC7901 and SGC-SS1,2 (SGC7901 transfected with scrambled control duplexes). Cell cycle analysis showed that proportions of MKN-calcyclin and SGC-SR1,2 cells in G0/ G1 and G2/M were significantly different compared to those of their control groups, respectively (P<0.05). The apoptosis rate of MKN-calcyclin was significantly lower compared to those of control groups (P<0.05). Results of colony-formation assay showed that the colony formation rate of MKN-calcyclin was higher compared to those of control groups, otherwise the rates of SGC-SR1,2 were lower compared to those of their control groups (P<0.05). The results of the cell migration assay showed that the migration rate of MKN-calcyclin was significant lower compared to those of its control groups, conversely, the migration rates of SGC-SR1,2 were significantly higher than those of their control groups (P<0.05). In conclusion, calcyclin can promote the growth and proliferation of gastric cancer cells and knockdown of calcyclin can restrain the growth and proliferation of gastric cancer cells. It can help tumor cells maintain the malignant phenotype. However, it can depress the ability of invasion of gastric cancer cells, thus restraining the metastasis of gastric cancer.

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“…Currently, a number of molecular abnormalities have been identified, including the activation of oncogenes, inactivation of tumor suppressor genes, microsatellite and chromosomal instability, and alteration of growth factors and cytokines (Smith et al, 2006). Many proto-oncogenes are activated and overexpressed in gastric cancer, such as c-met (Inoue et al, 2004), c-erB2 (Song et al, 2004), K-sam (Toyokawa et al, 2009), Ras (Nishigaki et al, 2005), and c-myc (Calcagno et al, 2005). Inactivation of tumor suppressor genes due to mutations and/or loss of heterozygosity is also a frequent event in gastric carcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

Bioinformatics analysis with graph-based clustering to detect gastric cancer-related pathways

Liu

Wang²,

Hu³

et al. 2012

Genet. Mol. Res.

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ABSTRACT. Despite a dramatic reduction in incidence and mortality rates, gastric cancer still remains one of the most common malignant tumors worldwide, especially in China. We sought to identify a set of discriminating genes that could be used for characterization and prediction of response to gastric cancer. Using bioinformatics analysis, two gastric cancer datasets, GSE19826 and GSE2685, were merged to find novel target genes and domains to explain pathogenesis; we selected differentially expressed genes in these two datasets and analyzed their correlation in order to construct a network. This network was examined to find graph clusters and related significant pathways. We found that ALDH2 and CCNB1 were associated with gastric cancer. We also mined for the underlying molecular mechanisms involving these differently expressed genes. We found that ECM-receptor interaction, focal adhesion, and cell cycle were among the significantly associated pathways. We were able to detect genes and pathways that were not considered in previous research on ©FUNPEC-RP www.funpecrp.com.br Genetics and Molecular Research 11 (3): 3497-3504 (2012) P. Liu et al. 3498 gastric cancer, indicating that this approach could be an improvement on the investigative mechanisms for finding genetic associations with disease.

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Interrelationship between chromosome 8 aneuploidy,C-MYCamplification and increased expression in individuals from northern Brazil with gastric adenocarcinoma

Abstract: Distinct patterns of alterations between intestinal and diffuse types of gastric tumors support the hypothesis that these types follow different genetic pathways.

Cited by 77 publications

References 36 publications

MYC and gastric adenocarcinoma carcinogenesis

MYC and gastric adenocarcinoma carcinogenesis

The role of calcyclin gene in the proliferation and migration of gastric cancer cells

Bioinformatics analysis with graph-based clustering to detect gastric cancer-related pathways

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