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Cancer > 4. The cell cycle and its regulation > Flashcards

4. The cell cycle and its regulation Flashcards

1
Q

Do embryonic or adult cells divide faster?

A

Embryonic

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2
Q

Do more or less complex systems divide more rapidly?

A

Less complex systems

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3
Q

Use 2 examples to show how the necessity for cell renewal determines the speed of division?

A
  • Intestinal epithelial cells - shed very often, renewal in 20 hours
  • Hepatocytes - renewal in 1 year
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4
Q

Most solid tumours are aneuploid, what does this mean?

A

Abnormal chromosome number and content

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5
Q

What mechanism involving the interaction with neighbouring cells to control growth is lost with tumour cells?

A

Contact inhibition

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6
Q

What 2 phases can the cell cycle be divided into?

A

Interphase (duplication) and mitosis (division)

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7
Q

What is the most vulnerable period of the cell cycle?

A

Mitosis - therefore it has to occur very quickly

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8
Q

Which part of the cell cycle is ideal for targeting tumour cells?

A

Mitosis (using clinical manipulation, irradiation, heat shock, chemicals)

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9
Q

How can DNA damage occurring during mitosis be repaired?

A

It can’t

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10
Q

At which phase are most cell in?

A

G0 (interphase) - cell cycle machinery is completely dismantled and normal cellular functions take place

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11
Q

What happens in the S phase?

A
  • DNA replication
  • Protein synthesis
  • Capacity for translation increased
  • Replication of organelles
  • Cell coordinates with replication of mitochondrial DNA
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12
Q

What is the centrosome and its functions?

A
  • Organelle near the nucleus which contains the centrioles
  • Microtubule organising centre (MTOC) - controls polymerisation of microtubules
  • Coordinates the mitotic spindle
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13
Q

What does the centrosome consist of?

A
  • 2 centrioles (mother and daughter centrioles) = barrels of 9 triplet microtubules
  • Matrix proteins hold the centrioles at 90 degree angles to each other
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14
Q

At which phase do the mother and daughter centrioles separate?

A

G1 phase

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15
Q

What happens to the mother and daughter centrioles once they separate, and in which phase does this take place?

A
  • They duplicate to reconstitute the perpendicular organisation of centrosomes
  • Mother produces a daughter centriole and daughter produces a mother centriole
  • S phase
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16
Q

What surrounds the centrioles?

A

Cloud of protein complexes

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17
Q

What happens when you put microtubules together and where does this take place?

A
  • Nucleation
  • Nucleating sites
  • When mitosis is needed, microtubules start to grow from these points and form an array of microtubules
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18
Q

What are the 6 different phases of mitosis?

A

1) Prophase
2) Prometaphase
3) Metaphase
4) Anaphase
5) Telophase
6) Cytokinesis

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19
Q

What happens in prophase?

A

CONDENSATION OF CHROMATIN (protection against breakage)

  • DNA strand beads onto a string involving histone proteins => chromatin
  • Chromatin further wrapped to form 30nm fibres
  • Fibres extended as a scaffold
  • Further wrapped => chromosome
  • Nuclear envelope breaks down
  • Chromosomes come out into the cytoplasm
  • Centrosomes migrate to opposite sides
  • Centrosomes organise the spindle
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20
Q

What’s in the middle of the chromosome?

A
  • Centromere - constriction around the chromosomes

* Kinetochore - protein complexes associated with the centromere, to which the microtubules of the spindle attach

21
Q

What are the 2 types of microtubule arrays that the centrosomes synthesise?

A

Radial microtubule arrays (asters)
• form around each centrosome
• start to form around the MTOC as soon as the nucleus starts to break down
• they grow and meet in the middle
• then hook to each other in the opposite direction, to form…

Polar microtubules
• form to stabilise structures
• microtubules between centrosomes

(astral microtubules continue to grow out in other directions)

22
Q

What happens in early prometaphase?

A
  • Breakdown of nuclear membrane is finalised
  • Spindle formation is largely complete
  • Attachment of chromosomes to spindle via kinetochores
23
Q

What happens in late prometaphase?

A
  • Microtubule from opposite pole is captured by sister kinetochore
  • CENP-E senses whether the kinetochore is attached
  • Captured chromosomes move to the middle of the cell
24
Q

What are the the 3 types of half-spindle?

A
  • Kinetochore microtubule - bound to the kinetochore
  • Polar microtubule - a microtubule that has met and connected with a microtubule from the other centrosomes
  • Astral microtubule - a microtubule that is originating from the centrosome that does not connect to a kinetochore
25
Q

What happens in metaphase?

A
  • Metaphase starts once kinetochore microtubules have attached to the kinetochores
  • Chromosomes are aligned at the equator of the spindle
26
Q

What happens in anaphase?

A
  • Cohesin is broken down and the microtubules get shorter (anaphase A)
  • Chromatids start moving towards the centrosomes
  • Spindle poles/centrosomes migrate apart (anaphase B)
  • The daughter chromatids are pulled towards opposite poles
27
Q

What happens in telophase and cytokinesis?

A
  • Daughter chromatids arrive at the poles
  • Nuclear envelope reassembles at each pole
  • Centrosomes are moved apart and cells try to revert to their normal size
  • Condensation of material where the cells are going to split
  • Assembly of contractile ring of actin and myosin filaments - at the midbody
  • Contractile ring squeezes the cell (cleavage furrow formed)
  • Cell divides
28
Q

What happens at the mitotic checkpoint?

A
  • CENP-E - protein from kinetochore that signals when it’s not attached to microtubules
  • BUB Protein Kinase - dissociates when chromatids are properly attached and signals progression into anaphase
29
Q

What is amphitelic attachment?

A

When the microtubule array of one centrosome is attached to the kinetochore of one sister chromatid, and the microtubule array of another centrosome is attached to the kinetochore of the other chromatid

30
Q

What is syntelic attachment?

A
  • Both kinetochores are hooked by 2 microtubule arrays from the same centrosome
  • Results in one cell having a duplication and the other cell having one less chromosome
31
Q

What is merotelic attachment?

A
  • There is more than one microtubule array attached to the same kinetochore
  • Chromatid is pulled in 2 different directions
  • Can result in a lost chromosome - both sister cells with have one less chromosome
32
Q

What is monotelic attachment?

A
  • Only one of the kinetochores of one chromatid is attached to a microtubule array
  • The other kinetochore is unattached
33
Q

What happens to mitosis in aberrant centrosome duplication?

A
  • If duplication is defective, you can end up with 4 centrosomes, not 2
  • Leads to abnormal attachment of the microtubule arrays
  • Abnormal cytokinese
  • Results in 4 daughter cells
34
Q

What happens to mitosis in aberrant DNA duplication?

A
  • Aberrant cytokinesis
  • 2 normal daughter cells
  • 2 cells with a single chromosome
  • 1 cell without any chromosome
35
Q

How do taxanes work?

A
  • Inhibit depolymerisation of microtubules
  • Disrupt microtubule function
  • Long-term mitotic arrest, tumour cells are disorganised and vulnerable - more easily killed
36
Q

How do vinca alkaloids work?

A
  • Inhibit polymerisation of microtubules
  • Produces unattached kinetochores
  • Long-term mitotic arrest - tumour cell more easily killed
37
Q

How can you exploit checkpoint control in cancer therapy (with ref. to kinetochores)?

A
  • Kinetochore signalling tells the cell when metaphase is complete
  • If you inhibit this checkpoint, you can make the nucleus think that it’s correctly hooked onto microtubules
  • Allows cells to proceed into anaphase prematurely
38
Q

How do CHEK1 + 2 inhibitors work?

A
  • Checkpoint kinase (CHEK1 + 2) - serine/threonine kinase
  • Normally, activation of this holds cells in G2 phase until all is ready
  • Inhibition leads to untimely transition to mitosis
  • Anaphase takes place too early => loss of chromosomes and cell death in tumour cells
39
Q

Describe 2 things that normally happen if something goes wrong during the cell cycle?

A

Cell cycle arrest
• mitosis stops and waits until problem is solved
• usually happens at checkpoints
• may be due to detection of DNA damage or cell not being big enough

Apoptosis
• DNA damage is too great and irreversible
• chromosomal abnormalities - cell can’t survive
• toxic agents

40
Q

Where does the cell enter the cell cycle (where growth factors are required)

A

G1 checkpoint

41
Q

Where is DNA damage checked before mitosis?

A

G2 checkpoint

42
Q

Apart from G1 and G2, what other checkpoint is there in the cell cycle?

A

Metaphase-anaphase checkpoint

43
Q

How can tumours exploit G1 checkpoint?

A
  • Hyper-activating growth factors
  • Over-express growth factors
  • Induces cell to overcome this checkpoint
  • Can also block DNA damage machinery - induces cell to enter mitosis when they shouldn’t
44
Q

How can the G0 phase be affected in tumour cells?

A
  • When cells divide, they pause and enter G0 - start functioning as normal cells
  • Tumours can block this - cycle is initiated and division continues
  • Causes hyper-proliferation
45
Q

Outline how a cell can leave the G0 phase via signalling cascades

A

• Response to extracellular factors
• Signal is relayed and modulated by other factors - signal amplification
• Signal diverges to reach multiple targets:
- regulation of metabolic pathway
- regulation of gene expression
- changes in cytoskeleton

46
Q

Describe 2 peptide growth factors and the activation of their receptor?

A

• Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) are dimeric
• Respective receptors are monomeric and found in the inactive state)
- Receptor Protein Tyrosine Kinase (RPTK)
• Ligand binds and activates the receptor - dimerisation of the receptors
• Activates the kinase domain
• Cross-phosphorylation of receptors due to kinase domains being brought close together
• Phosphorylated amino acid residues in the kinase domain => activation

47
Q

Describe the protein phosphorylation by protein kinase, and reversal

A

• Protein kinase transfer phosphate from ATP to hydroxyl group of amino acids
- One type phosphorylates serine + threonine
- Another type phosphorylates tyrosine
• Phosphate group (negative) causes change in conformation - change in activity, and creates a docking site for another protein
• (Serine) phosphorylation is a signalling trigger
• Reversed by protein phosphatase

48
Q

Outline the protein kinase cascade

A
  • First kinase activated by phosphorylation
  • Further kinases activated by activated kinases
  • Other types of proteins can be phosphorylated e.g. scaffolding proteins and transcription factors
49
Q

How can you tackle tumorigenesis with reference to the protein kinase cascade

A

Inhibit the kinases

Cancer (15 decks)

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