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Cancer and The Cell Cycle > Cell cycle control > Flashcards

Cell cycle control Flashcards

1
Q

In the yeast model, what is the name for the cdk controlling entry into mitosis?

A

Cdc2

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2
Q

In the yeast model, what is the name for the cyclin controlling entry into mitosis?

A

Cdc13

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3
Q

In the yeast model, which enzyme phosphorylates the Cdk (Cdc2) at its inhibitory site?

A

Wee1

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4
Q

Which enzyme phosphorylates Cdk (Cdc2) at its activating site?

A

CAK (Cdk-activating kinase)

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5
Q

Which enzyme removes the inhibitory phosphate group from Cdk (Cdc2)?

A

Phosphorylated (i.e. ACTIVE) Cdc25 phosphatase

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6
Q

How is the phosphatase Cdc25 activated?

A

Positive feedback: the active Cdc2/Cdc13 (i.e. Cdk/Cyclin) complex phosphorylates Cdc25

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7
Q

How are the levels of cyclin controlled during the cell cycle?

A

Proteasomal destruction

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8
Q

What are CKIs?

A

Cdk inhibitor proteins

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9
Q

Give two examples of CKIs

A

p16

p21/27

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10
Q

Give an example of a CKI for:
Cdk4/6
Cdk2/Cyclin E

A

1) p16

2) p21/27

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11
Q

How are levels of cyclin D regulated throughout the cell cycle?

A

Activated by growth factors/ mitogens

Inhibited by growth inhibitors/ anti-mitogens

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12
Q

How are levels of Cdk-inhibitors regulated throughout the cell cycle?

A

Inhibited by growth factors/mitogens

Activated by growth inhibitors/anti-mitogens

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13
Q

Give 7 ways in which Cdk/Cyclins can be regulated

A
  1. CKIs binding to Cdk along
  2. Proteosomal degradation of cyclins
  3. Phosphorylation of Cdk
  4. Binding of cyclin
  5. Binding of CKI to Cdk/cyclin
    etc
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14
Q

Which is the G1/S cyclin?

A

Cyclin D

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15
Q

Which are the two cyclins involved in the S phase? Which is involved in transition into the S phase, and which is involved in continuing the S phase?

A

Cyclin E and Cyclin A

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16
Q

Which cyclin is involved in the S/G2 transition?

A

Cyclin A

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17
Q

Which cyclin is involved in the G2/M transition?

A

Cyclin B

18
Q

In what order are the cyclins synthesised?

A

Cyclin D
Cyclin E
Cyclin A
Cyclin B

19
Q

When are each of the cyclins synthesised?

A

Cyclins D, E and A are synthesised during G1 phase.

Cyclin B is synthesised during the S phase

20
Q

When are each of the cyclins broken down? How are they broken down?

A

They are ubiquitinylated and thus targeted for degradation.
Cyclin E is degraded in S phase
Cyclins A, B and D are degraded in mitosis

21
Q

In what order are the cyclins degraded?

A

EABD

22
Q

What are the four main cell cycle checkpoints? When do they occur?

A
  1. Restriction point checkpoint - G1
  2. DNA damage checkpoint - G1/S transition
  3. DNA replication stress response - G2/S
  4. Mitotic spindle assembly checkpoint - Mitosis
23
Q

Cancer arises through loss of cell cycle checkpoints. What are these, and what is the result of loss of each?

A
  1. Loss of restriction point checkpoint: continuous proliferation of cells
  2. Loss of DNA damage checkpoint: accumulation of genetic damage (mutations), chromosome breakage and fusion
  3. Loss of DNA replication stress response: loss of genetic material, mutations, breakage of chromosomes
  4. Loss of mitotic spindle assembly checkpoint: chromosome segregation errors, aneuploidy and chromosome instability
24
Q

Traditional cancer treatments target all dividing cells including both cancer and normal cells. Give some examples of such treatments, and where they affect the cell cycle.

A

1) Anti-metabolites - stop cells making the building blocks of DNA during G1 - e.g. methotrexate, 5-FU
2) Agents binding to DNA - stop DNA synthesis during S phase - e.g. alkylating agents
3) Microtubule inhibitors - stop cells making components needed to separate during G2 - include vincristine etc.

25
Q

Give an example of a microtubule inhibitor

A

Vincristine

26
Q

Give an example of an anti-metabolite

A

5-FU / methoxatrine

27
Q

Give an example of an agent that binds to DNA to prevent DNA synthesis

A

Alkylating agents/ platinum compounds

28
Q

Give three examples of drugs used as traditional cancer treatments

A

Microtubule inhibitors (e.g. vincristine)
Anti-metabolites (e.g. 5-FU)
Agents that bind to DNA to prevent DNA synthesis (e.g. alkylating agents)

29
Q

Why have traditional cancer treatments that are aimed at killing dividing cells effective in adults but not children?

A

Because in an adult, most cells are not dividing

30
Q

What are the serious side effects that result from treating cancer by killing off all dividing cells? List 4.

A

1) Nausea, vomiting, diarrhoea (gut epithelia)
2) Immune suppression (immune cells)
3) Anaemia (erythrocyte precursors)
4) Hair loss (hair follicle cells)

31
Q

Why can traditional cancer treatments that target ALL dividing cells have serious side effects such as nausea, immune suppression, anaemia and hair loss?

A

Because some normal adult cells continue to divide, e.g. gut epithelia, immune cells, erythrocyte precursors and hair follicle cells

32
Q

Traditional cancer treatments cause some serious side effects. How could treatment be changed to avoid these?

A

By finding specific target molecules that are absent or present at much lower levels in normal cells compared to tumour cells
OR
Exploit the fact that cancer cells have defects in checkpoint pathways

33
Q

What is a tumour?

A

Large mass of cells that has lost control over proliferation

34
Q

Which cell cycle checkpoint must be lost in order for a tumour to develop?

A

The restriction point checkpoint during G1

35
Q

Cancer involves loss of control over cell proliferation. What else does it depend on?

A

Accumulation of genetic damage

36
Q

The integrity of which cell cycle checkpoints must be lost in order for a cell to accumulate genetic damage?

A

1) DNA damage checkpoint

2) mitotic spindle assembly checkpoint

37
Q

Rapidly dividing cells suffer from replication stress. What can a failure to deal with this lead to?

A

Increased genetic damage

38
Q

Which cell cycle checkpoint controls cell proliferation?

A

The restriction point

39
Q

Which kinases control passage through the restriction point?

A

Cyclin D-dependent kinases (Cdk4 and Cdk6)

40
Q

Yeast genetics identified a network of genes required for mitotic entry. What were these, and which transition did they control?

A

G2-M
Cdc13 (the mitotic cyclin) binds to active Cdc2 (a cyclin dependent kinase). Cdc2 is phosphorylated at both its activating site and its inhibitory site by Cdk-activating kinase (CAK) and Cdk-inhibitory kinase (wee1). The inhibitory phosphate is then removed by the phosphatase Cdc25, and the Cdk/Cyclin (Cdc2/Cdc13) complex becomes active

Cancer and The Cell Cycle (2 decks)

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