Down‐regulation of <i>drs</i> mRNA in Colorectal Neoplasms

Mukaisho, Ken‐ichi; Suo, Masashi; Shimakage, Misuzu; Kushima, Ryoji; Inoue, Hirokazu; Hattori, Takanori

doi:10.1111/j.1349-7006.2002.tb01334.x

Cited by 10 publications

(9 citation statements)

References 34 publications

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“…This protein has one transmembrane domain, a short intracellular domain in the C-terminus and three consensus repeats (sushi motifs) conserved in the extracellular domain among the selectin family of adhesion molecules and complementbinding proteins (Bevilacqua et al, 1989;Johnston et al, 1989;Reid and Day, 1989;Siegelman et al, 1989;Norman et al, 1991;Lasky, 1992;Kansas, 1996). We also showed that the expression of drs mRNA is markedly downregulated in a variety of human cancer cell lines and malignant tumor tissues, including those of the colon, bladder, ovary, lung, and prostate (Yamashita et al, 1999;Shimakage et al, 2000;Mukaisho et al, 2002;Shimakage et al, 2002;Kim et al, 2003). Introduction of drs cDNA by retrovirus vector into these cancer cell lines suppressed anchorage-independent growth without disturbing cell proliferation.…”

Section: Introductionmentioning

confidence: 91%

A novel apoptotic pathway induced by the drs tumor suppressor gene

et al. 2004

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The drs gene was originally isolated as a suppressor against v-src transformation. Expression of drs mRNA was markedly downregulated in a variety of human cancer cell lines and tissues, suggesting that the drs gene acts as a tumor suppressor. In this study, we found that ectopic expression of the Drs protein induced apoptosis in human cancer cell lines. Analyses using deletion mutants of drs revealed that both the C-terminal region and the three consensus repeats in the N-terminal region are essential for the induction of apoptosis. Caspase-12, -9, and -3 were sequentially activated by drs, and specific inhibitors of caspase-3 and -9 suppressed drs-induced apoptosis. The release of cytochrome c from the mitochondria into the cytoplasm was not observed in apoptosis by drs, suggesting that the mitochondrial pathway does not mediate drsinduced apoptosis. Furthermore, we found that the Drs protein can interact with ASY/Nogo-B/RTN-x S , an apoptosis-inducing protein localized in the endoplasmic reticulum, and that coexpression of these genes increased the efficiency of apoptosis. These results indicated that Drs induces apoptosis by a novel pathway mediated by ASY/Nogo-B/RTN-x S , caspase-12, -9, and -3.

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Section: Introductionmentioning

confidence: 91%

A novel apoptotic pathway induced by the drs tumor suppressor gene

et al. 2004

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“…At least three of the chromosome X genes, SLC25A5, SRPX, and RBBP7, which were differentially expressed in any of the EOC cell lines relative to NOSE samples, were also differentially expressed in a comparative HuGeneFL array analysis of low malignant potential ovarian tumors and malignant EOC samples (32). SRPX expression was also downregulated in various cancers including lung (42), colorectal (43), and prostate (44) carcinomas. SRPX was shown to suppress anchorage-independent growth in in vitro assays using a number of human cancer cell lines including an ovarian cell line (45).…”

Section: ------------------------------------------------------------mentioning

confidence: 97%

Global analysis of chromosome X gene expression in primary cultures of normal ovarian surface epithelial cells and epithelial ovarian cancer cell lines

Benoît

Hudson²,

Maire³

et al. 2007

Int J Oncol

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The interpretation of loss of heterozygosity (LOH) in cancers is complicated as genes that map to LOH regions may be transcriptionally active (Xa) or inactive (Xi) due to X chromosome inactivation (XCI). We have analyzed the chromosome X transcriptome in four epithelial ovarian cancer (EOC) cell lines (TOV21G, TOV81D, TOV112D, and OV90) and 12 primary cultures of normal ovarian surface epithelial (NOSE) cells in relation to chromosome X integrity. Two-way comparative analysis using HuGeneFL Affymetrix GeneChips ® of TOV21G, TOV81D and OV90 relative to the NOSE samples was highly correlated (>89%) in contrast to that of TOV112D (56-69%). TOV112D, followed by TOV21G, exhibited the largest number of up-regulated genes. XIST expression by RT-PCR was not detectable in TOV112D or TOV21G. Allele-specific transcription by cDNA sequence analysis of genes known to be subjected to XCI revealed maintenance of XCI in TOV81D and OV90, but not TOV21G. Biallelic expression could not be assessed in TOV112D due to reduction to hemizygosity of chromosome X. Chromosome X rearrangements were observed in FISH analysis of TOV112D and TOV21G, and both of these EOC cell lines were negative for Barr body analysis. The differentially expressed genes did not appear to map to any particular region of the X chromosome in any EOC cell line. The absence of XIST expression is consistent with Barr body loss in TOV112D and TOV21G. The combined evidence is consistent with two proposed mechanisms to account for absence of Xi in female cancers: Xi loss followed by Xa duplication (exemplified by TOV112D) and transcriptional reactivation of Xi (exemplified by TOV21G). Despite an alteration in XIST expression and differences in allelic content in the EOC cell lines, the chromosome X transcriptome was modified modestly when compared with that of NOSE samples.

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“…In the present study, downregulation of the expression of SRPX and FLNC was identified, which probably was inhibited by miR-200c-5p or miR-16-5p and miR-205-5p, respectively. SRPX was firstly isolated as a novel transformation suppressor gene, and SRPX expression is downregulated by retroviral oncogenes such as v-src or v-ras (26). Research has demonstrated that SRPX expression is markedly reduced in various human cancer cell lines (26,27).…”

Section: Deg Between Risk Groups ------------------------------------mentioning

confidence: 99%

“…SRPX was firstly isolated as a novel transformation suppressor gene, and SRPX expression is downregulated by retroviral oncogenes such as v-src or v-ras (26). Research has demonstrated that SRPX expression is markedly reduced in various human cancer cell lines (26,27). Tambe et al documented that the C-terminal region and the 3 consensus repeats in the N-terminal region of SRPX are critical in SRPX-induced apoptosis.…”

Section: Deg Between Risk Groups ------------------------------------mentioning

confidence: 99%

Exploration of bladder cancer molecular mechanisms based on miRNA-mRNA regulatory network

Liu

Zou

et al. 2017

Oncology Reports

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To explore the complex molecular mechanisms of bladder cancer, mRNA and miRNA expression profiles were combined for systematic analyses. A total of 18 common differentially expressed genes (DEGs) were identified from two mRNA expression datasets which consisted of 206 tumor and 74 normal tissues. Then, survival analysis based on the SurvExpress database showed that the common DEGs were able to significantly differentiate low- and high-risk groups in 4 public bladder cancer datasets (p<0.01). Notably, the tumor and normal samples were able to be almost clearly classified into 4 groups based on these identified common DEGs. In addition, 6 out of the 18 common DEGs, including ALDH1A1 and SRPX, are regulated by 6 reported miRNAs based on regulatory network analyses. Expression levels of the 6 DEGs were validated in 10 bladder cancer samples using RT-PCR, and the expression values were concordant with the microarray results. Collectively, our analyses indicated that various biological processes are involved in the development and progression of bladder cancer. Firstly, cell cycle checkpoints and DNA repair networks of cancer stem-like cells were regulated by high expression of ALDH1A1, and hence promoted tumor self-renewal or metastasis. Then, activation of HspB6 induced the angiogenesis process which provides necessary nutrition and oxygen for tumor cells. Moreover, downregulation of the expression of tumor-suppressor genes SRPX and FLNC further promoted apoptosis and metastasis. The identification of potential biological processes and genes can be helpful for the understanding of bladder cancer molecular mechanisms.

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Down‐regulation of drs mRNA in Colorectal Neoplasms

Cited by 10 publications

References 34 publications

A novel apoptotic pathway induced by the drs tumor suppressor gene

A novel apoptotic pathway induced by the drs tumor suppressor gene

Global analysis of chromosome X gene expression in primary cultures of normal ovarian surface epithelial cells and epithelial ovarian cancer cell lines

Exploration of bladder cancer molecular mechanisms based on miRNA-mRNA regulatory network

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