Skin tests with autologous cholesteryl hemisuccinate treated tumour cells in cancer patients

1985 ◽  
Vol 20 (2) ◽  
pp. 179-181 ◽  
Author(s):  
Marta Munzarová ◽  
Daniela Zemanová ◽  
Jan Kovařik ◽  
Aleš Rejthar
Keyword(s):  
Cancer Patients ◽  
Tumour Cells ◽  
Skin Tests ◽  
Cholesteryl Hemisuccinate ◽  
Treated Tumour

Long-term Follow-up of Bladder Cancer Patients with Disseminated Tumour Cells in Bone Marrow

2011 ◽  
Vol 60 (2) ◽  
pp. 231-238 ◽  
Author(s):  
Margitta Retz ◽  
Jens Rotering ◽  
Roman Nawroth ◽  
Alexander Buchner ◽  
Michael Stöckle ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Bladder Cancer ◽  
Cancer Patients ◽  
Tumour Cells ◽  
Long Term Follow Up ◽  
Disseminated Tumour Cells

scholarly journals Metformin Impairs Glutamine Metabolism and Autophagy in Tumour Cells

Cells ◽  
2019 ◽  
Vol 8 (1) ◽  
pp. 49 ◽  
Author(s):  
Serena Saladini ◽  
Michele Aventaggiato ◽  
Federica Barreca ◽  
Emanuela Morgante ◽  
Luigi Sansone ◽  
...  
Keyword(s):  
Apoptotic Cell ◽  
Tumour Cells ◽  
Glutamine Metabolism ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Ammonia Accumulation ◽  
Tumour Cell Lines ◽  
Type 2 Diabetic ◽  
Treated Tumour

Metformin has been shown to inhibit glutaminase (GLS) activity and ammonia accumulation thereby reducing the risk of hepatic encephalopathy in type 2 diabetic patients. Since tumour cells are addicted to glutamine and often show an overexpression of glutaminase, we hypothesize that the antitumoral mechanism of metformin could be ascribed to inhibition of GLS and reduction of ammonia and ammonia-induced autophagy. Our results show that, in different tumour cell lines, micromolar doses of metformin prevent cell growth by reducing glutamate, ammonia accumulation, autophagy markers such as MAP1LC3B-II and GABARAP as well as degradation of long-lived proteins. Reduced autophagy is then accompanied by increased BECN1/BCL2 binding and apoptotic cell death. Interestingly, GLS-silenced cells reproduce the effect of metformin treatment showing reduced MAP1LC3B-II and GABARAP as well as ammonia accumulation. Since metformin is used as adjuvant drug to increase the efficacy of Cisplatin-based neoadjuvant chemotherapy, we co-treated tumour cells with micromolar doses of metformin in the presence of cisplatin observing a marked reduction of MAP1LC3B-II and an increase of caspase 3 cleavage. In conclusion, our work demonstrates that the anti-tumoral action of metformin is due to the inhibition of glutaminase and autophagy and could be used to improve the efficacy of chemotherapy.

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