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Biology Of Cancer > Regulation Of Cell Proliferation And Death > Flashcards

Regulation Of Cell Proliferation And Death Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

Which tissues do not proliferate?

A

Skeletal muscle

Nerves

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2
Q

What happens in each phase of the cell cycle?

A

G1 - metabolic changes prepare the cell for division

S - DNA synthesis replicates the genetic material - each chromosome now consists of two sister chromatids

G2 - metabolic changes assemble the cytoplasmic materials necessary for mitosis and cytokinesis

M - nuclear division (mitosis) followed by cellular division (cytokinesis)

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3
Q

Functions of checkpoints?

A

Check the cell is ok to proliferate
Check the previous phase is completed
Check it is timely
Check for DNA damage

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4
Q

Which tissues have a high turnover of cells?

A

Skin
Haemopoietic tissue
Gut mucosa

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5
Q

What do cyclin-dependent kinases (CDKs) do?

A

Regulate the cell cycle, transcription and mRNA processing by phosphorylation proteins at serine and threonine.

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6
Q

How does the activity of CDKs change throughout the cycle and why?

A

Oscillates throughout the cycle

Depends on the availability of cyclins

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7
Q

What are cyclins?

A

Short-lived proteins degraded by the ubiquitin-proteasome pathway

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8
Q

Which CDKs and cyclins are present at the G1 checkpoint?

A

Cyclin D with CDK 4-6

Cyclin E with CDK2

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9
Q

Which CDKs and cyclins are present at the G2/M checkpoint?

A

CDK1 and cyclin B

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10
Q

Why is it useful to know which CDKs and cyclins are present?

A

Can help to determine which stage of the cell cycle a cell is in

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11
Q

What does the retinoblastoma protein (pRb) do normally?

A

It is a tumour suppressor gene

Prevents excessive cell growth by inhibiting cell cycle progression from G1 to S until a cell is ready to divide

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12
Q

What happens if both alleles for the retinoblastoma protein are mutated?

A

It is inactivated leading to retinoblastoma

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13
Q

How does pRb stop cell cycle progression?

A

Prevents replication of DNA by recruiting HDA1C, causing deacetylation of histones
Rb is phosphorylated to pRb by CDKs which inactivates it, allowing the cell cycle to progress

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14
Q

What happens to pRb as the cell cycle progresses?

A

From M1 to G1, it is progressively dephosphorylated, retiring to its active state as Rb

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15
Q

What do E2F target genes code for?

A

A family of transcription factors involved in cell cycle regulation and synthesis of DNA

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16
Q

What do the different transcription factors that the E2F target gene code for do?

A

Three allow cell cycle progression

Six are suppressors

17
Q

What is the order of cells in the crypts of the small intestine?

A

Paneth cells
Stem cells are just above
Proliferating progenitor cells occupy the rest of the crypt

18
Q

Which cells populate the villi of the small intestine?

A

Differentiated cells
Goblet cells
Enterocytes
Entero-endocrine cells

19
Q

Where do cells proliferated and differentiate in the small intestine

A

Progenitor cells proliferate in the crypts

They differentiate in the villi

20
Q

Which pathway regulates the proliferation of progenitor cells in the small intestine?

A

WNT pathway

21
Q

What happens as the proliferating cells reach the mid-crypt area?

A

Beta-catenin/TCF activity is down-regulated, causing cell cycle arrest and differentiation

22
Q

What does APC do?

A

It is a tumour suppressor gene which degrades beta catenin (beta-catenin promotes progenitor cell proliferation)

23
Q

What does WNT do?

A

Prevents degradation of beta-catenin, promoting cell proliferation in the crypts

24
Q

What happens if there is a mutation to the APC gene?

A

Beta-catenin is not broken down so cells in the surface epithelium ccontinue to behave as crypt progenitor cells, resulting in polyps

25
Q

What does MPF (mitosis-promoting factor) do?

A

It sensors negative signals of incomplete replication

Phosphorylates multiple substrates to trigger entry into mitosis

26
Q

How are cyclin-dependent kinase complexes inactivated, stopping mitosis?

A

If there is a double strand break, ATM is activated
If there is a single strand break, ATR is activated
They activate WEE1, which inactivates the complex by phosphorylation

27
Q

Other than inactivating CDK-cyclin complexes, what else can ATM and ATR phosphorylate?

A

p53 - can be phosphorylated, increasing its activity

28
Q

Functions of p53?

A

Growth arrest - holds cell cycle at G1/S checkpoint if there is DNA damage

DNA repair - activates DNA repair proteins

Apoptosis - if DNA damage is irreparable

29
Q

What does Mdm2 do?

A

It is an oncogene

Binds to and inactivates p53 - transports it to the cytoplasm via ubiquitin system

30
Q

How is Mdm2 and p53 regulated?

A

Expression of Mdm2 is activated by p53
Mdm2 can only break down p53 when p53 is not phosphorylated
p53 is phosphorylated by ATM/ATR which increase when there is DNA damage
Mdm2 also increases but cannot break it down
When damage is fixed, ATM/ATR are deactivated and mdm2 can then break down p53

31
Q

What does P14RF do?

A

Binds to mdm2 and inhibits it, inhibiting degradation of p53
Activates pRb
Therefore has a dual tumour suppressive effect

32
Q

How can the intrinsic pathway of apoptosis be triggered?

A

Viral infection

Damage to DNA from toxins, free radicals or radiation

33
Q

What happens in the intrinsic pathway?

A

P53 blocks Bcl-2 proteins
They cause release of cytochrome C from mitochondria by formation of pores in mitochondrial membrane
Cytochrome C forms an apoptosome with APAF-1
This activates a cascade of caspases that cause the cell to die
Caspase-3 is the effector caspase (protease enzymes)

34
Q

How is the extrinsic pathway activated?

A 
A ligand e.g. 
-FasL
-TNF-α
-ΤRAIL
binds to a death receptor e.g.
-Fas
-TNFR1
-DR5
on the cell surface
35
Q

Where is TRAIL expressed?

A

Cell surface of T cells

36
Q

What happens when a ligand binds to a death receptor to activate the extrinsic pathway of apoptosis?

A

Recruitment of FADD (Fas-associated protein with death domain) and caspases 8 and 10
Fas and caspase 8 form DISC (death-inducing signalling complex)
Caspase 8 activates caspase 3 which is the effector caspase, causing cell death
Leads to a death-inducing cytoplasmic signalling complex

37
Q

What role does p53 have in the extrinsic pathway?

A

Activates transcript of death receptors and caspase 8

38
Q

How does p53 decide whether to induce apoptosis or just arrest the cell cycle?

A

Depends on the amount and types of protein present

  • p21 has a high affinity so if there is not a lot of p53 present, get cell cycle arrest
  • Bax has a lower affinity for p53, so if there is lots of p53 present, it causes apoptosis

Biology Of Cancer (13 decks)

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