Q2. What are the main components of the arginine metabolites?
They metabolize L-arginine with the enzymes arginase and nitric oxide synthase (NOS) generating products that inhibit the function of infiltrating lymphocytes and, in addition, depriving lymphocytes of arginine.
Q3. What are the contributions in "From tumor cell metabolism to tumor immune escape" ?
Villalba et al. this paper suggested that changes in tumor cell metabolism may propel tumor cell immune escape.
Q4. What is the role of miRNAs in regulating glutamine metabolism?
miRNAs play a central role in regulating posttranscriptional gene expression by annealing to the 3‟ untranslated regions of target mRNAs to generally promote mRNA degradation or translational repression (Chhabra et al., 2010).
Q5. What is the role of p65 in the regulation of glutamine metabolism?
cells growing in glutamine increase p65 translocation to the nucleus where it controls glutamine metabolism by downregulating miR-23a levels.
Q6. What is the role of LXRs in tumor cell metabolism?
In addition, LXRs are also implicated in PNT formation and therefore can affect T cell activation as described above (Russo, 2011).
Q7. What is the effect of ATP-citrate lyase on tumor growth?
in absence of ATP-citrate lyase, which ensures the production of acetyl-CoA from citrate, global histone acetylation is reduced.
Q8. What is the effect of fermentation on tumor cells?
fermentation is much quicker than respiration on producing ATP and offers a selective advantage to rapidly growing tumor cells.
Q9. What is the main characteristic of tumor cell metabolism?
In summary, the Warburg effect, which is currently called aerobic glycolysis because of the increase rate of glycolysis in the presence of oxygen, is not the only feature of tumor cell metabolism.
Q10. What is the main “fuel” used by mitochondria?
a certain quantity of pyruvate, the main “fuel” used by mitochondria, still enters the tricarboxylic acid (TCA) cycle for bioenergetic and biosynthetic purposes (Levine and Puzio-Kuter, 2010).
Q11. What is the effect of DCA on pyruvate dehydrogenase?
DCA inhibits pyruvate dehydrogenase kinase isozyme 1 (PDK1; (Whitehouse et al., 1974) and, therefore, activates pyruvate dehydrogenase isozyme 1 (PDH1; (Bartrons and Caro, 2007).
Q12. What is the effect of GTN on prostate cancer?
The results suggest that GTN has a consistent, inhibitory effect on prostate-specific antigen (PSA)-expressing tumor progression in men with recurrent prostate cancer after primary treatment failure.
Q13. What are the main reasons for the tumor metabolic shift?
tumor metabolic shift is probably due to several processes including overexpression of glycolytic enzymes and metabolite transporters, defects in cellular respiration and oncogenic alterations.
Q14. Why does the study show a clinical benefit in patients with cancer?
a clinical benefit is observed in a low number of patients, probably because tumors produce some immunomodulators that block CTL activity (see above).
Q15. What is the role of MHC-I in tumors?
The expression of one or more of these proteins is often altered in tumor cells, leading to a decrease of surface expression of MHC-I.
Q16. What is the role of MUC1 in tumors?
This is a general overview because some adhesion molecules, such as like mucin-1 (MUC1), are usually overexpressed in tumors and functions as a TAA (Pashov et al., 2010).
Q17. What is the effect of a decrease in extracellular pH?
More than this, because cellular lactate secretion via monocarboxylate transporters (MCTs) is accompanied by H + transport, a decrease in extracellular pH results in a reduction of CTL function due to intracellular accumulation of lactate (Fischer et al., 2007,Dietl et al., 2010).
Q18. What is the link between tumor cell metabolism and tumor cell development?
tumor cell metabolism is most likely linked to tumor cell development because several waves of gene regulation constantly modify the metabolism during tumorigenesis (Smolkova et al., 2011).
Q19. What is the effect of phagocytes on cholesterol efflux?
this cholesterol efflux was not observed when engulfed cells trigger inflammatory signaling (i.e. Fc Receptor engagement or necrosis sensing) suggesting that cholesterol load may depend on inflammatory condition encountered by the phagocytes.