Glutamine metabolism in the avian host bearing transplantable hepatomatous growth induced by MC-29 virus

Matsuno, Tomonori; Satoh, Teikichi

doi:10.1016/0020-711x(86)90155-2

Cited by 14 publications

(1 citation statement)

References 7 publications

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“…Previous studies have shown that GLS1 expression is upregulated in gliomas, colorectal carcinomas, adenomas, and breast cancer cell lines [ 15 – 17 ]. It has also been shown that GLS1 and GLS2 activities were increased approximately 20-fold and 6-fold, respectively, in transplanted hepatomas [ 18 , 19 ]. Similar results were obtained in various hepatoma cells of human and rat origin in cultured form or in ascitic form [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Kidney-type glutaminase (GLS1) is a biomarker for pathologic diagnosis and prognosis of hepatocellular carcinoma

Shi

et al. 2015

Oncotarget

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The lack of sensitive and specific biomarkers hinders pathological diagnosis and prognosis for hepatocellular carcinoma (HCC). Since glutaminolysis plays a crucial role in carcinogenesis and progression, we sought to determine if the expression of kidney-type and liver-type glutaminases (GLS1 and GLS2) were informative for pathological diagnosis and prognosis of HCC. We compared the expression of GLS1 and GLS2 in a large set of clinical samples including HCC, normal liver, and other liver diseases. We found that GLS1 was highly expressed in HCC; whereas, expression of GLS2 was mainly confined to non-tumor hepatocytes. The sensitivity and specificity of GLS1 for HCC were 96.51% and 75.21%, respectively. A metabolic switch from GLS2 to GLS1 was observed in a series of tissues representing progressive pathologic states mimicking HCC oncogenic transformation, including normal liver, fibrotic liver, dysplasia nodule, and HCC. We found that high expression of GLS1 and low expression of GLS2 in HCC correlated with survival time of HCC patients. Expression of GLS1 and GLS2 were independent indexes for survival time; however, prognosis was predominantly determined by the level of GLS1 expression. These findings indicate that GLS1 expression is a sensitive and specific biomarker for pathological diagnosis and prognosis of HCC.

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Section: Introductionmentioning

confidence: 99%

Kidney-type glutaminase (GLS1) is a biomarker for pathologic diagnosis and prognosis of hepatocellular carcinoma

Shi

et al. 2015

Oncotarget

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Prominent glutamine oxidation activity in mitochondria of avian transplantable hepatoma induced by MC‐29 virus

Matsuno

Satoh

Suzuki

1986

Journal Cellular Physiology

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Well coupled mitochondria were isolated from transplantable chicken hepatoma induced by MC-29 virus. The mitochondrial phosphate-dependent and phosphate-independent glutaminase activities were increased compared with those from normal chicken liver. Glutamate dehydrogenase was undetectable in the tumor mitochondria. Oxypolarographic tests showed the following: glutamine oxidation was prominent in the tumor mitochondria and was mediated through an NAD-linked reaction, while mitochondria from the liver showed a feeble glutamine oxidation; glutamine oxidation by tumor mitochondria was inhibited either by aminooxyacetate, inhibitor of transaminases, or prior incubation of mitochondria with DON (6-diazo-5-oxonorleucine), which inhibited mitochondrial glutaminases. Bromofuroate, inhibitor of glutamate dehydrogenase, had little or no effect; and glutamate oxidation was also inhibited by aminooxyacetate, while it was not affected by DON. These findings clearly show a high glutamate oxidation activity in the hepatoma and indicate that the product of glutamine hydrolysis, glutamate, is catabolized via transamination in the mitochondria to supply ATP.

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Production of tumor growth‐inhibiting protein by the neonatal mouse brain: Dependence on intracellular glutamine metabolism

Miwa

Matsuno

Mizuno

1987

Journal Cellular Physiology

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We previously reported that the mouse brain at the neonatal stage but not at the adult stage secreted a carcinostatic factor of 62,000 Da, termed NBCF, which inhibited clonal growth and DNA synthesis of malignant cells preferentially over those of normal cells. In the present study, NBCF production by the neonatal mouse brain in culture was investigated. Addition of L-glutamine to the culture medium markedly promoted NBCF production in a concentration-dependent manner. The production seemed to be specific to glutamine, since no promotive effect was exerted by L-glutamic acid, its analogue DL-alpha-aminoadipic acid, L-aspargine, or L-aspartic acid or by other amino acids or vitamins. NBCF production was markedly reduced in culture medium either devoid of L-glutamine or containing 6-diazo-5-oxo-L-norleucine, a glutamine antagonist, or L-methionine sulfoximine, an inhibitor of glutamine synthetase. Thus NBCF production was promoted by extracellular supply, intracellular synthesis, and utilization of L-glutamine but was not affected by its deamidated form or homologue amino acids. On the other hand, NBCF production was completely repressed by addition of cycloheximide to the culture medium. The repressive effect was also exerted by actinomycin D although not completely, whereas cytosine beta-D-arabinofuranoside did not repress NBCF production. These results indicated that NBCF production by cultivation was independent of DNA replication but dependent mostly on a transcription stage and its following stages and partly on a translation stage from the preexisting mRNA to the protein.

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Glutamine metabolism in the avian host bearing transplantable hepatomatous growth induced by MC-29 virus

Cited by 14 publications

References 7 publications

Kidney-type glutaminase (GLS1) is a biomarker for pathologic diagnosis and prognosis of hepatocellular carcinoma

Kidney-type glutaminase (GLS1) is a biomarker for pathologic diagnosis and prognosis of hepatocellular carcinoma

Prominent glutamine oxidation activity in mitochondria of avian transplantable hepatoma induced by MC‐29 virus

Production of tumor growth‐inhibiting protein by the neonatal mouse brain: Dependence on intracellular glutamine metabolism

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