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CancerGen > Cell Cycle > Flashcards

Cell Cycle Flashcards

1
Q

Our cells are in what homeostasis?

A

Between cell division and cell death

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2
Q

What does too much cell division lead to?

A

Cancer

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3
Q

What does too much cell death lead to?

A

organ sculpting

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4
Q

What two main groups of proteins are important in the cell cycle?

A

Kinases and Phosphatases

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5
Q

What does CDK stand for?

A

Cyclin Dependent Kinase

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6
Q

What do CDKs do?

A

Drive the cell cycle, each at different stages.

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7
Q

What do CDKs need to be active to drive the cell cycle?

A

A cyclin

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8
Q

Cyclin-CDK complexes can be regulated in what two main ways?

A

Inhibitors, or they get phosphorylated by proteins like Wee1 that can inactivate them. Other phosphorylation can activate them.

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9
Q

Which cyclin CDK complex drives commitment into the cell cycle?

A

cyclin D-CDK4

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10
Q

What are the main stages of the cell cycle in order?

A

Can have a G0, otherwise G1, into S, then G2, then M.

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11
Q

When is cyclin D expression activated?

A

In response to growth factors/mitogens

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12
Q

What do E2F transcription factors do?

A

Drive expression of genes needed to enter the S-phase

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13
Q

Why can’t E2F TFs generally push a cell into the S phase?

A

Rb is inhibiting E2F in the absence of growth factors

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14
Q

How is Rbs inhibition of E2F released in the presence of growth factors?

A

Growth factors lead to cyclin D expression. CyclinD-CDK4 inhibits Rb. So E2F can then activate expression of genes to enter S-phase.

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15
Q

What type of gene is Rb? And how?

A

Retinoblastoma is a tumour supressor gene. It ensures cells only enter the cell cycle in the presence of growth factors.

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16
Q

What happens when Rb is faulty?

A

There is unstimulated proliferation of the cell be E2F TFs are uninhibited.

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17
Q

What is P27’s role in the regulation of CyclinD-CDK4?

A

It is an inhibitor that binds to the complex. But when P27 is phosphorylated, that lifts the footbrake, letting the complex act again.

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18
Q

Which signalling pathway phosphorylated the footbrake P27?

A

Ras-MAPK

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19
Q

How does cyclinD-CDK4 ensure that the cell cycle is fully commited?

A

By hyperphosphorylation of Rb, it’s all or nothing.

20
Q

What is TGFbeta’s role in the cell cycle?

A

It can be a brake or a promoter of the cell cycle. Sometimes it upregulates inhibitors leading to cell cycle arrest, somethings it stimulates progression through promoting expression of CDKs and cyclins.

21
Q

Upon detection of DNA damage, what happens to P53?

A

P53 gets stabilised and thus activated.

22
Q

What does P53 do to halt the cell cycle?

A

Activates P21 that binds to and inhibits cyclin-CDK complexes. This causes G1 arrest.

23
Q

If there is too much DNA damage in a cell what does P53 lead to?

A

Cell death.

24
Q

Cyclin D is not needed in breast development. But what is true of breast cancer?

A

HER2 breast cancer needs cyclin D function…

25
Q

CDK4 is needed for what cancer?

A

K-ras induced lung tumours

26
Q

What complex does the drug Palcyclib mimic?

A

The INK4 complex that inhibits cyclinD-CDK4

27
Q

Overexpression of the MYC proto-oncogene doesn’t lead to cancer in mice pancreas cells. Why?

A

Those cells died. But if you inhibit apoptosis too, then you cancer. Driving proto-oncogenes is not enough.

28
Q

What is necrosis?

A

Inflammatory cell lysis

29
Q

What is autophagy?

A

A cell eating itself

30
Q

What is apoptosis?

A

Efficient, controlled cell death

31
Q

What is extrinsic apoptosis briefly?

A

Apoptosis triggered by cell surface receptors

32
Q

What is intrinsic apoptosis briefly?

A

Apoptosis triggered by DNA damage or misfolded proteins.

33
Q

What proteins increase when there’s a lot of DNA damage or overexpression of oncogenes?

A

BH3 only proteins

34
Q

What protein family are inhibited when there’s lots of DNA damage or overexpression of oncogenes?

A

BCL-2 pro-survival proteins is inhibited

35
Q

What proteins lead to mitochondrial signalling?

A

BAX and BAK.

36
Q

At some point there’s an apoptotic switch. What proteins are then activated?

A

Caspase 9 and effector caspases.

37
Q

Explain the apoptotic trigger?

A

DNA damage leads to P53 upregulation which leads to transcription of noxa/puma (BH3 only proteins). They neutralise the effect of BCL2 family.

38
Q

List 4 BH3 only proteins?

A

Bid, Bim. Puma, Noxa

39
Q

The BH3 domain is in which proteins?

A

The BH3 only proteins, the BCL2 anti-apoptotic family, and BAX and BAK proapoptotic proteins.

40
Q

What do the BH3 only proteins do?

A

They interact with the BH3 domain in the BCL2 proteins, so that they can’t bind to the proapoptic proteins BAX and BAK and sequester them.

41
Q

What is the apoptotic switch starting with BAX and BAK?

A

BAX and BAK form oligomers in the mitochondrial outer membrane. MOMP (pores) form, signalling moelcules come out, leading to the formation of the apoptosome which activate caspases leading to apoptosis

42
Q

What is the apoptosome made of?

A

APAF-1 and cytochrome C.

43
Q

What are the different types of caspases?

A

Initiators - activated by proximity, oligomerisation.
Executioner - Activated by cleavage.

44
Q

What are BH3 mimetics?

A

It’s when in therapy we are trying to reactivate apoptosis in oncogenic cells by inhibiting BCL2, BCL-W and BCL-XL.

45
Q

Why was targeting BCL-XL good in research but bad in patients?

A

BCL-XL is also needed for platelets. So targeting this had unexpected toxicity in patients.

46
Q

How could we improve BCL-XL targeted BH3 mimetics?

A

Targeting to directly to the tumour so it doesn’t affect the blood.

CancerGen (18 decks)

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