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Summary reader Molecular Regulation Of Health and Disease (HAP-31806)

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Summary of the reader of the course Molecular Regulation Of Health and Disease (HAP-31806)

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  • 19 maart 2021
  • 26
  • 2020/2021
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Reader Summary Molecular Regulation of Health and Disease

1. MOLECULAR REGULATION OF ENERGY AND NUTRIENT METABOLISM
Difference cancer cells compared to normal cells:
 Immortal
 Display sufficiency in growth signals
 Are invasive and have properties that support invasion and metastasis
o Have loss of contact inhibition
o Have reduced cellular adhesion
o Have loss of anchorage dependence
o Have less organized, more mobile surface proteins
o Show an altered secreted protein profile
 Are resistant to programmed cell death
 Have an altered nutrient and energy metabolism
o Show an increased rate of glycolysis
o Have a more negative surface charge of the cell membrane and sustained
angiogenesis

Cancer cells are re-programmed such that optimal growth
of the individual cell is facilitated, but at the expense of
the organism to which the cancer cell belongs

Hallmarks of cancer:
 Sustaining proliferative signalling
 Evading growth suppressors
 Resisting cell death
 Enabling replicative immortality
 Inducing angiogenesis
 Activating invasion and metastasis
 Evading immune destruction
 Reprogramming of energy metabolism

Cancer cell metabolism is programmed to optimize cell
growth, this means that a major goal of cancer cells is to produce the three major constituents of the
cell: protein, DNA and membranes. The major fuels that are consumed by cancer cells are glucose,
glutamine and fatty acids. ATP, NADH and NADPH are needed for all catabolic and anabolic processes
to proceed

Mitochondria:
 organelles that reside in eukaryotic cells
 have a double membrane (the mitochondrial outer membrane (MOM) and the mitochondrial
inner membrane (MIM))
 Mitochondria have their own circular DNA
 Mitochondrial DNA encodes for 13 proteins of the 1250 that are in it. The others are encoded
by nuclear DNA and imported into mitochondria via the so-called TOM (translocator of outer
membrane) and TIM (translocator of inner membrane) complexes
 Functions:
o Produce ATP
o Respond to cellular energy requirements
o Regulate the balanced use of energy substrates in:
 The urea cycle

,  Calcium homeostasis
 Amino acid metabolism
o Essential for heme and ironsulpur cluster biosynthesis
o Mediation of apoptosis and innate immune defence
o Oxidative signalling mediated by reactive oxygen species (ROS)
 Mitochondria functions are substantially altered in cancer cells

Glycolysis:
 Anaerobic
 Provides 2 ATP per molecule glucose
 High capacity/low efficiency system
 End product can be 2 molecules of pyruvate, which are imported into mitochondria, or 2
molecules of lactate
o Pyruvate enters the TCA cycle
o TCA cycle breaks down acetyl CoA to generate CO 2 and reduce NAD+ to NADH and
FAD to FADH2
o Providing electrons to the electron transport complex (ETC)
 The electrons are moved from complex to complex
 Creating an electrochemical proton gradient
 Resulting into ATP synthesis
 Oxidative Phosphorylation (OXPHOS)
 Generating 32-34 ATP per glucose

Reactive oxygen species (ROS):
 The free radicals that are generated because of OXPHOS
 Unpaired electrons
 Interaction of unpaired electrons with O 2 results in the generation of superoxide ions (O 2-)
 Potentially harmful
 Enzymatic systems to inactivate ROS:
o Copper-Zinc Superoxide Dismutase
o Manganese Superoxide Dismutase
o Catalase (peroxisome) and glutathione peroxidases
 Vitamins C and E have an important role in protection against ROS
 ROS may cause lipid peroxidation and damage to cell membranes and to DNA
 ROS is thought to be formed at complex I, II, and III, when electrons cannot be transferred to
the next complex
o When mobile carriers Co-enzyme Q and cytochrome
C cannot deliver their electrons and are thus are fully
occupied with electrons
 An imbalance between the generation of ROS and the cell’s
ability to clear oxidants can lead to pathogenic levels of ROS
leading to damage of proteins, lipids, and DNA

Apoptosis is determined through two main interconnected
pathways, which are the:
 Intrinsic pathway
o Receptor mediated
o Involving tumour necrosis factor receptors (TNFR)
 FAS (CD95)
 TRAIL (TNFRSF10)
o Extracellular domain binds to ligand

,  Leading to receptor clustering and intracellular recruitment of proteins into a
death-inducing signalling complex (DISC)
 Which then activates an initiator caspase, pro-caspase 8 (or 10)
 Triggering the execution phase of apoptosis via the activation of the
downstream effector caspase, Caspase 3 (and 6, 7)
 Extrinsic pathway
o Can be activated by cellular stresses
o Activation of the intrinsic pathway results in mitochondrial permeabilization
 Release of pro-apoptotic proteins
 Loss of the mitochondrial (trans) membrane potential (ΔΨm) and
concomitant arrest of the bioenergetic function of the organelle
 Two protein categories:
 Proteins that can activate the caspase dependent pathway
 Other cell death proteins such as apoptosis inducing factor (AIF) and
endonuclease G (Endo G)

Processes that contribute to mitochondrial outer membrane permeabilization (MOMP) and thereby
promote the translocation of mitochondrial intermembrane space proteins:
 Prolonged opening of the permeability transition pore (PTP)
 Channel formation by pro-apoptotic proteins BAX and BAK1
 Direct MOMP effects of pro-apoptotic stimuli

Resistance to apoptosis:
 thought to be caused by deregulation of several master switch proteins such as:
o Hypoxia inducible factor-1 (HIF1),
o c-Myc
o TP53
 Results in:
o The upregulation of anti-apoptotic proteins
o Suppression of pro-apoptotic proteins
o Silencing of death receptors
o Production of hexokinase II (HKII), which increases the resistance of mitochondrial
permeability transition (MPT)

To prevent cell death, cells have many specific repair and waste disposal/recycle pathways. Cancer
cells adopt and fine-tune these pathways to maintain cell proliferation.

Lysosomes play a central role in waste disposal and recycling pathways
 Single membrane organelles
 Form an acidic compartment
 Involved in cell signalling, membrane repair,
immune response and energy metabolism

Damaged or dysfunctional proteins can be removed by:
 Ubiquitin mediated proteosomal degradation
 Chaperone mediated autophagocytosis
o Proteins are directed to the lysosome

Lysosomal degradation is also used for breakdown of
components that are taken up by:
 Endocytosis

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