Mitochondrial adenosine triphosphatase in the oxyphil cells of a renal oncocytoma

Hunter, V.Ross; Pauly, Daniel F.; Wolkowicz, Paul E.; McMillin, Jeanie B.; Beckner, Marie E.

doi:10.1016/0046-8177(90)90207-l

Cited by 6 publications

(3 citation statements)

References 26 publications

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“…Moreover, these tumors show limited growth [27]. A mitochondrial origin was previously suggested for this pathology [28], although the levels of some OXPHOS enzymes are normal in these tumors [10,29]. Histochemical investigations of renal oncocytomas have shown decreased activity of the pentose phosphate pathway enzyme glucosed-phosphate dehydrogenase and a corresponding increase in the activity of the glycolytic enzyme GAPDH in these tumors [30,31].…”

Section: Discussionmentioning

confidence: 97%

Expression of oxidative phosphorylation genes in renal tumors and tumoral cell lines

et al. 1996

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To investigate the regulation of genes encoding the proteins involved in energy metabolism in cancer cells, we studied the expression of several mitochondrial and nuclear genes involved in ATP production. Northern blot analysis was performed on renal tumors of different types: a clear cell carcinoma, an oncocytoma, and urothelial tumors at two different stages. The steady-state transcript patterns were compared with those observed in cell lines derived from renal tumors and in transformed cell lines. Striking differences were revealed among the three types of tumors, their respective controls, and the cultured renal cells. The levels of all mitochondrial transcripts were lower in tumor biopsies and tumoral cell lines than in the normal cell types. Moreover, a higher transcript level of nuclear genes involved in oxidative phosphorylation was observed in the oncocytomas and in the more malignant urothelial tumor. Different transcript patterns were observed in each of the tumoral and transformed cell lines, explaining the difference in metabolism between the different tumors and the tumoral or transformed cell lines. In particular, a high transcript level for the adenine nucleotide translocator isoform 2(ANT2) gene, which is usually not expressed in differentiated cells, was observed in oncocytoma and malignant urothelial renal tumor. This phenomenon was also observed in renal carcinoma cell lines and transformed cells. These data provide the first argument for the involvement of the ANT2 protein in glycolytic ATP uptake in cancer cell mitochondria and suggest a possible ANT2 antisense strategy for cancer therapy.

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Section: Discussionmentioning

confidence: 97%

Expression of oxidative phosphorylation genes in renal tumors and tumoral cell lines

et al. 1996

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“…Numerous key components of the oxidative phosphorylation machinery have been identified histochemically or immunohistochemically in oncocytic lesions of the thyroid, kidney, parathyroid gland and salivary gland [28,46,58,62,90], but only a partial deficiency of cytochrome-C-oxidase in oncocytic nodules of hyperplastic or adenomatous parathyroid glands has been found [58]. Oncocytes have traditionally been regarded as cells with active metabolism and high levels of oxidative enzymes [90].…”

Section: Unravelling the Pathogenesismentioning

confidence: 99%

Oncocytic tumours

Tallini¹

1998

Virchows Archiv

145

131

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Oncocytic tumours represent a distinctive set of lesions with distinctive granular cytoplasmic eosinophilia of the neoplastic cells. These cells are called oncocytes because of the "swollen" appearance they have as the result of a striking accumulation of mitochondria. Although generally uncommon, oncocytic tumours are by no means rare and have been reported, with different frequencies, in virtually every organ. A variety of biochemical and molecular changes have been identified, and the aberrant biogenesis of mitochondria in oncocytic cells bears intriguing similarities to that of a group of degenerative disorders known as mitochondrial encephalomyopathies. Although the relationship between the accumulation of mitochondria and the occurrence of tumours is unknown, investigation into the cellular alterations of oncocytes may further our knowledge of a variety of important biological processes such as proliferation, energy production and ageing.

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“…An investigation conducted by Oh et al showed that there was no association between aspirin use and lung cancer risk with the pooled odds ratio (OR) 0.86 (95% confidence interval (CI) 0.76–0.98). [10] Xu et al also, performed a meta-analysis which showed aspirin use with a dose of 7 tablets per week can significantly reduce lung cancer risk (pooled OR 0.80, 95%CI: 0.67–0.95), whereas non-aspirin NSAIDs showed no chemopreventive value. [11] Meta-analysis by Jiang et al reported that aspirin do not display protective effect of regular aspirin use on lung cancer risk.…”

Section: Introductionmentioning

confidence: 99%

Non-steroidal anti-inflammatory drugs and risk of mortality in lung cancer

Chen

Kang²,

Zhu³

et al. 2019

Medicine

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Background: Non-steroidal anti-inflammatory drugs (NSAIDs) especially aspirin has been gained increasing attention due to its potential therapy against to lung cancer. Previous investigations have showed different findings in this issue. We studied the safety profile and efficacy of NSAIDs in treating lung cancer. Method: Embase, Pubmed, and Cochrane Library databases were searched from January 2011 to February 2019. We identified the studies meeting a priori inclusion criteria and it also conducted a secondary review. This meta-analysis of 5 prospective studies was launched to evaluate the effect of NSAIDs for patients with lung cancer on the hazard risk (HR). We used the Random-Effect Model to assess pooled HR and between-study heterogeneity. Application of subgroup analysis, meta-regression, as well as sensitivity analysis was to pinpoint the exact sources of the observed heterogeneity. Results: 5 Prospective Cohorts Studies, including 6017 patients with lung cancer were recruited in the final meta-analysis. In general, using of NSAIDs especially aspirin is not associated with mortality of lung cancer: pooled hazard ratio (HR) of 0.88 [95% confidence intervals (CI): 0.73–1.05] with low heterogeneity (Q = 6.95; I 2 = 42.4%, P = .139). Egger ( P = .665) and Begg ( P = 1.000) test also showed little trial error in this meta-analysis. Conclusion: NSAIDs did not increase the risk of mortality in patients with lung cancer.

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Mitochondrial adenosine triphosphatase in the oxyphil cells of a renal oncocytoma

Cited by 6 publications

References 26 publications

Expression of oxidative phosphorylation genes in renal tumors and tumoral cell lines

Expression of oxidative phosphorylation genes in renal tumors and tumoral cell lines

Oncocytic tumours

Non-steroidal anti-inflammatory drugs and risk of mortality in lung cancer

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