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, Gerald P.

doi:10.1002/(sici)1097-0215(19970516)71:4<565::aid-ijc10>3.0.co;2-b

Cited by 17 publications

(9 citation statements)

References 16 publications

(10 reference statements)

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“…Table II shows the base pair length of amplified cDNA of 6 genes under study and the sequence of sense and antisense primers to amplify those cDNAs (37).…”

Section: Construction Of Gene-specific Primersmentioning

confidence: 99%

“…To confirm differential expression of the 6 genes under study, gene-specific probes were generated by gene-specific RT-PCR technique (37). Different amounts of cDNAs and several PCR cycles were used to generate gene-specific probes.…”

Section: Gene-specific Rt-pcr Analysismentioning

confidence: 99%

“…Differentially expressed gene-specific DNA bands were then eluted from the gel and purified with the help of the QIAquick Gel Extraction kit (Qiagen, Inc., Valencia, CA). These genespecific DNA bands were used as a probe in Northern blot (37).…”

Section: Gene-specific Rt-pcr Analysismentioning

confidence: 99%

“…Human ß-actin control amplifier set probe was also used in northern hybridization to confirm their similar expression in all the samples. The blot was then exposed to Kodak X-OMAT AR film at -80˚C for 24 h. Intensity was assessed by densitometric scanning (Molecular Dynamics, NJ) (36,37).…”

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

confidence: 99%

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Profiling of cell cycle genes of breast cells exposed to etodolac

Roy

Arason²,

Chowdhury³

et al. 2010

Oncol Rep

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Abstract. Breast cancer represents the second leading cause of cancer-related deaths in the world. There is increasing evidence that perturbation of cell cycle regulation is an important contributing factor to various cancer progression stages. There are key checkpoints in the cell cycle involving various regulatory proteins. The relationship between these cell cycle regulatory proteins and cell cycle arrest by cyclooxygenase (COX) inhibitors during neoplastic progression remains largely unknown. Preclinical studies and epidemiological investigations have consistently shown that nonsteroidal anti-inflammatory drugs have some anti-proliferative and anti-oxidative stress response on various tumors. In this study, the effect of etodolac, a 1,8-diethyl-1,3,4,9-tetrahydropyrano (3,4-ß) indole-1-acetic acid on signaling pathways was investigated by examining the differential expression of various cell cycle regulatory protein genes. A human cell cycle gene array was used to profile the expression of 96 genes involved in the cell cycle regulation. Differentially expressed genes were highly altered by etodolac treatment. Twenty-six genes were up-and 20 down-regulated with 0.5 and 2 mM etodolac treatment, respectively. Seven genes (ATM, BAX, CCNA2, CDC27, RAD50 and p21) were prominently altered, and six (ATM, CCND2, CCNF, CDC20, CDK1A and RAD50) were commonly altered with both concentrations. This finding indicated that etodolac could play a critical role on cancer cells by inducing cell death. IntroductionBreast cancer represents the second leading cause of cancerrelated deaths in the United States and other Western countries; accounting for about 30-40% of all newly diagnosed cancers (1,2). Hereditary breast cancer accounts for just 5-10% of cases. It is generally believed that a family history of breast cancer and hormonal imbalances also contributes to the development of breast cancer (3,4). The etiology of breast cancer remains unknown, however, a profound and diverse number of factors including developmental, genetic, nutrition, chemotherapy, hormones, the environment and other yet undetermined factors have been implicated as risk factors for mammary tumorigenesis (5-8).The malignant breast cell phenotype develops as a result of a multi-step process, requiring multiple genetic mutations (9-12). These mutations contribute to a cell that is increasingly characterized by uncontrolled proliferation, deregulated production of growth factors, non-responsiveness to extracellular anti-proliferative signals, anchorage independence, metastatic potential and resistance to antineoplastic agents. Recent advances in the molecular biology of breast cancer have identified various genes associated with tumorigenesis (13,14). The development and progression of neoplastic transformation and the experimental reversal of tumorigenicity are accompanied by complex changes in patterns of gene expression. Complicated events are required for normal cells to change their behavior and these events involve the interaction between genes and pos...

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“…Table II shows the base pair length of amplified cDNA of 6 genes under study and the sequence of sense and antisense primers to amplify those cDNAs (37).…”

Section: Construction Of Gene-specific Primersmentioning

confidence: 99%

Section: Gene-specific Rt-pcr Analysismentioning

confidence: 99%

Section: Gene-specific Rt-pcr Analysismentioning

confidence: 99%

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

confidence: 99%

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Profiling of cell cycle genes of breast cells exposed to etodolac

Roy

Arason²,

Chowdhury³

et al. 2010

Oncol Rep

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“…Differential display allows the mRNA profile of all genes expressed from two different samples to be compared side by side, on the same gel, making the simultaneous detection of both up-and downregulated gene expression possible . This technique has been widely used in studying up-or downregulated genes in many tumour tissues, including prostate, thyroid (Musholt et al, 1997), pancreatic (Ozaki et al, 1998), and breast cancers (Watson and Fleming, 1994), colorectal and oesophageal carcinomas (Graber et al, 1996;Chan et al, 1998), melanoma (Duncan et al, 1998), and glioblastoma (Chuaqui et al, 1997;Sehgal et al, 1997). However, to our knowledge, no study using this technique in primary SCCHN tissues has been performed, although a few studies have reported using mouse or tumour cell lines of SCCHN (Gorogh et al, 1997;Patel et al, 1997;Gottschlich et al, 1999;Dong et al, 2001).…”

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confidence: 99%

Preferential expression of hPGFS in primary SCCHN and tumour cell lines derived from respiratory and digestive organs

Hanna

Breau

et al. 2004

Br J Cancer

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Identifying overexpressed genes in tumours is a critical step for tumour diagnosis, prognosis, and treatment. Using differential display polymerase chain reaction, sequence analysis, and gene Blast searches, we discovered that human prostaglandin F synthase (hPGFS) was upregulated in squamous cell carcinoma of the head and neck (SCCHN). Northern blot analysis indicated that up to a 16-fold increase in the level of hPGFS expression was detected in 40.5% (15 out of 37) of SCCHN primary tumours. The increased expression of hPGFS in SCCHN was primarily detected in SCC of larynx and hypopharynx (59%, Po0.05). Using the same primary tissue samples, increased levels of epidermal growth factor receptor (EGFR) expression were detected in only 32% of tumour tissues, suggesting hPGFS may have the potential to become a drug target or molecular marker for SCCHN. To determine if the increased level of hPGFS expression came from tumour cells, we determined the level of hPGFS expression in SCCHN tumour cell lines. A high level of hPGFS expression was detected in four out of five tumour SCCHN cell lines. To determine if upregulation of hPGFS is SCCHN-specific, hPGFS expression was analysed in 59 tumour cell lines derived from different types of tumours. The expression of hPGFS was increased from two-to 500-fold in a large portion of cell lines derived from lung (five out of nine), colon (five out of seven) as well as head and neck cancer (four out of five). These data link hPGFS expression to tumours located in the respiratory and digestive organs.

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Cloning, sequence, and developmental expression analysis of C4-2, a potential brain tumor-suppressor gene

et al. 1997

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Background Previously, we reported the isolation of C4‐2 as a potential tumor suppressor gene in human brain tumors. To understand the function of this gene, we investigated its molecular characterization and expression during development. Methods Human fetal brain library screening and 5′RACE‐PCR method was used to isolate the full‐length cDNA. The coding region of C4‐2 was used for in situ hybridization to study its expression during development. Results We report here the complete sequence of this gene. Sequence analysis indicated that C4‐2 has a 94% sequence identity to a family of cAMP‐regulated phosphoproteins (ARPP‐16/19) in the coding region. C4‐2 has a 3.1 Kb long 3′UTR with variable identity to ARPP‐16 and ARPP‐19. Northern blot analysis indicated that C4‐2 is expressed at high levels in normal brain compared to other tissues. Zoo blot analysis demonstrated that the coding region of C4‐2 is highly conserved among different animals. In situ hybridization using C4‐2 coding region demonstrated that it follows a unique expression pattern during mouse brain development. High level of C4‐2 expression was also observed in the spinal cord and somites of the developing embryo. Conclusion Expression analysis during brain development strongly suggests that this family of proteins may play an important role not only in normal functioning of the brain, but also during brain development. J. Surg. Oncol. 1997;65:249–257. © 1997 Wiley‐Liss, Inc.

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

Cited by 17 publications

References 16 publications

Profiling of cell cycle genes of breast cells exposed to etodolac

Profiling of cell cycle genes of breast cells exposed to etodolac

Preferential expression of hPGFS in primary SCCHN and tumour cell lines derived from respiratory and digestive organs

Cloning, sequence, and developmental expression analysis of C4-2, a potential brain tumor-suppressor gene

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