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In this presentation, we will describe part of the mechanisms
that are involved in the reprogramming of oxidative phosphorylation in cancer.
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The talk is going to be structured in four main parts.
First, we will look at the tight connection that exists between
oxidative phosphorylation and glycolysis to explain metabolic reprogramming in cancer.
Next, we will study the mechanisms that control
oxidative phosphorylation at the level of the ATP synthase in cancer.
And there are two main mechanisms;
by limiting the content of the ATP synthase,
and by inhibiting the activity of the ATP synthase,
by a small mitochondrial protein that is called IF1,
and it is the ATPase inhibitory factor one.
The third part of the talk,
will be devoted to the regulation of the activity of this inhibitor.
And finally, we will look at the role of the F1 ATPase in cancer progression,
and specifically focused on IF1.
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Oxidative phosphorylation is the mitochondrial pathway
for obtaining biological energy in the form of ATP.
In this process, the electrons that have been obtained in the oxidation
of glucose and fatty acids are collected in NADH,
which is going to transfer the electrons to
the respiratory change that is placed in the inner mitochondrial membrane.
Electrons flow down through these complexes to
molecular oxygen to generate the water of respiration.
In this electron transfer through the respiratory complexes,
the proteins pump protons from
the matrix of the mitochondria into the intermembrane space,
generating what is called the proton electro-chemical gradient.
Another protein also placed in the inner mitochondrial membrane,
that is called the ATP synthase,
is going to utilize the proton gradient to generate the ATP that is used by the cell,
by the phosphorylation of the ADP and inorganic phosphate
that is made available to the matrix of the organelle by specific transporters.
