Isolation and characterization of a novel gene from human glioblastoma multiforme tumor tissue

Sehgal, Anil; Keener, Cassie L.; Boynton, Alton L.; Young, Ronald F.; Vermeulen, Sandra; Yonemura, Kenneth S.; Kohler, Erik P.; Aldape, Hector C.; Simrell, Charles R.; Murphy, G.P.

doi:10.1002/(sici)1097-0215(19970516)71:4<565::aid-ijc10>3.3.co;2-5

Cited by 4 publications

(8 citation statements)

References 9 publications

(14 reference statements)

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“…Another target gene, RAB3D, is a member of RAS oncogene family and upregulated in several different tumor types with potential oncogenic function, including lung cancer. [43][44][45] In this study, we did observe high expression of RAB3D in lung cancer tissues. Thus, miR-1262 also might down-regulate RAB3D expression and then play the role of tumor suppressor gene in lung cancer.…”

Section: Discussionsupporting

confidence: 53%

A polymorphism in miR‐1262 regulatory region confers the risk of lung cancer in Chinese population

Xie

Chen

Zhu

et al. 2017

Intl Journal of Cancer

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It has been proposed that the majority of disease-associated loci identified by genome-wide association studies (GWAS) are enriched in non-coding regions, such as the promoter, enhancer or non-coding RNA genes. Thus, we performed a two-stage case-control study to systematically evaluate the association of genetic variants in miRNA regulatory regions (promoter and enhancer) with lung cancer risk in 7,763 subjects (discovery stage: 2,331 cases and 3,077 controls; validation stage: 1,065 cases and 1,290 controls). As a result, we identified that rs12740674 (C > T) in miR-1262 enhancer was significantly associated with the increased risk of lung cancer (additive model in discovery stage: adjusted OR = 1.31, 95%CI = 1.13-1.53, p = 3.846 × 10 in Nanjing GWAS; adjusted OR = 1.20, 95%CI = 1.00-1.44, p = 0.041 in Beijing GWAS; validation stage: adjusted OR = 1.20, 95%CI = 1.03-1.41, p = 0.024). In meta-analysis, the p value for the association between rs12740674 and lung cancer risk reached 6.204 × 10 (adjusted OR = 1.24, 95%CI = 1.13-1.36). Using 3DSNP database, The Cancer Genome Atlas (TCGA) data and functional assays, we observed that the risk T allele of rs12740674 reduced the expression level of miR-1262 in lung tissue through chromosomal looping, and overexpression of miR-1262 inhibited lung cancer cell proliferation probably through targeting the expression levels of ULK1 and RAB3D. Our findings confirmed the important role that genetic variants of noncoding sequence play in lung cancer susceptibility and indicated that rs12740674 in miR-1262 may be biologically relevant to lung carcinogenesis.

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Section: Discussionsupporting

confidence: 53%

A polymorphism in miR‐1262 regulatory region confers the risk of lung cancer in Chinese population

Xie

Chen

Zhu

et al. 2017

Intl Journal of Cancer

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“…Normal tissues such as thyroid, stomach, adrenal cortex, small intestine and pancreas show high expression of D2-2. D2-2 is expressed 28 times higher in fetal brain (20 weeks) than in adult brain [58]. Sequence analysis of a 2.0-Kb fragment for D2-2 shows no homology to known sequences in the database.…”

Section: Overexpression Of D2-2mentioning

confidence: 94%

Molecular changes during the genesis of human gliomas

Sehgal

1998

Semin. Surg. Oncol.

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Neoplastic transformation in the normal human brain occurs as a result of the accumulation of a series of genetic alterations. These genetic alterations include the loss, gain or amplification of different chromosomes which lead to altered expression of proteins that play important roles in the regulation of cell proliferation. Several common genetic alterations at the chromosomal level (loss of 17p, 13q, 9p, 19, 10, 22q, 18q and amplification of 7 and 12q) have been observed. These alterations lead to changes in the expression of several genes; protein 53 (p53), retinoblastoma (RB), interferon (INF)α/β, cyclic AMP dependent kinase number 2 (CDKN2), mutated in multiple advanced cancers 1 (MMAC1), deleted‐in‐colon carcinoma (DCC), epidermal growth factor receptor (EGFR), platelet derived growth factor (PDGF), platelet derived growth factor receptor (PDGFR), MDM2, GLI, CDK4 and SAS during the genesis and progression of human gliomas. Recent studies suggest that altered expression of several other genes ]MET; MYC; transforming growth factor β (TGFβ); CD44; vascular endothelial growth factor (VEGF); human neuroglial‐related cell adhesion molecule (hNr‐CAM); neuroglial cell adhesion molecule (NCAM L1); p21waf1/Cip1; TRKA; mismatch repair genes (MMR); C4‐2; D2‐2[ and proteins ]e.g., cathepsins, tenascin, matrix metalloproteases, tissue inhibitors of metalloproteases, nitric oxide synthase, integrins, interleukin‐13 receptor (IL‐13R), Connexin43, urokinase‐type plasminogen activator receptors (uPARs), extracellular matrix proteins and heat shock proteins[ are associated with the genesis of human gliomas. Taken together, these findings point to the accumulation of multiple genetic mutations coupled with extensive changes in gene expression in the etiology of human gliomas. Semin. Surg. Oncol. 14:3–12, 1998. © 1998 Wiley‐Liss, Inc.

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“…As a control, we demonstrate that the expression of a tumor-associated gene (D2-2) is high in GMT compared to NBT (Fig. 2) [16]. D1-2, a control gene that was isolated from a similar batch of DD-PCR, is expressed consistently at the same levels in normal and tumor samples.…”

Section: Isolation Of Clone C4-2 Using Technique Of Modified Dd-pcrmentioning

confidence: 63%

“…As shown in Figure 4, C4-2 was expressed at very low levels in glioblastoma, meningiomas, colon cancer metastatic to the brain, recurrent glioma, B-cell lymphoma, breast tumors, prostate tumors, and a prostate tumor cell line (LNCAP). Clone D2-2 was used as a control overexpressed gene from brain tumors to illustrate the integrity of the experiments [16]. This experiment confirmed that low expression of C4-2 was not only confined to brain tumor tissues but also to other tumor types.…”

Section: Expression Of C4-2 In Tumor Tissuesmentioning

confidence: 65%

Characterization of C4-2 as a tumor-suppressor gene in human brain tumors

et al. 1997

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Background Brain tumors claimed the lives of 13,300 people in 1995. Our objective was to isolate and characterize unique tumor‐suppressor genes from human brain tumors derived from patients in the United States. Methods Differential display‐polymerase chain reaction was used to isolate tumor suppressor genes. Results Clone C4‐2 was isolated and is expressed in normal adult human brain, but not in brain tissue from glioblastoma multiforme tumors. C4‐2 has 66% homology to the previously isolated ARPP‐16 (cAMP‐regulated phosphoprotein of Mr = 16,000) based on limited sequencing. C4‐2 is expressed at high levels in normal brain and is not expressed or expressed at low levels in several brain tumor cell lines. Expression of C4‐2 was also either not expressed or expressed at low levels in meningioma, B‐cell lymphoma, recurrent glioma, LNCAP (prostate tumor cell line), breast tumor, or prostate tumor tissue. Conclusion We conclude that C4‐2 may function as a potential tumor‐suppressor gene. J. Surg. Oncol. 64:102–108 © 1997 Wiley‐Liss, Inc.

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Isolation and characterization of a novel gene from human glioblastoma multiforme tumor tissue

Cited by 4 publications

References 9 publications

A polymorphism in miR‐1262 regulatory region confers the risk of lung cancer in Chinese population

A polymorphism in miR‐1262 regulatory region confers the risk of lung cancer in Chinese population

Molecular changes during the genesis of human gliomas

Characterization of C4-2 as a tumor-suppressor gene in human brain tumors

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