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hallmarks of cancer > evading apoptosis > Flashcards

evading apoptosis Flashcards

1
Q

what is apoptosis

A

programmed cell death which removes damaged, unwanted or diseased cells. it is highly regulated and does not damage neighbouring cells

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2
Q

2 examples of overactive apoptosis

A

neurodegeneration and immunodeficiency

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3
Q

2 examples of underactive apoptosis

A

cancer and inflammatory conditions

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4
Q

physiological use of overactive apoptosis in normal cells

A

returns cell population to normal after challenge

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5
Q

physiological use of underactive apoptosis in normal cells

A

allows cell accumulation (immune response)

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6
Q

what happens to the cell in necrosis

A

cell swelling, organelle disruption, nuclear swelling and plasma membrane rupture

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7
Q

what happens to the cell in apoptosis

A

cell shrinkage, organelles stay intact, chromatin condensation, plasma membrane integrity is kept

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8
Q

cons of necrosis

A

its messy so cell contents are leaked into surroundings, could cause signal issues

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9
Q

how long does it take for apoptosis to occur

A

30-120 mins

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10
Q

3 examples of where messages for intrinsic apoptosis come from

A

DNA damage, ER stress and hypoxia

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11
Q

example of where messages for extrinsic apoptosis come from

A

death receptors on surface of the cell

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12
Q

2 main apoptosis routes

A

intrinsic and extrinsic

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13
Q

where does the message come from in intrinsic apoptosis

A

inside the cell

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14
Q

where does the message come from in extrinsic apoptosis

A

outside the cell

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15
Q

where does the name Caspases derive from

A

Cysteine ASPartate specific proteASES

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16
Q

what do caspases do

A

cut a specific protein sequence, where they cut is defined by a tetrapeptide

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17
Q

what is a tetrapeptide

A

4 amino acids

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18
Q

what are inflammatory caspases responsible for

A

the maturation of pro-inflammatory cytokines

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19
Q

what are initiator caspases responsible for

A

starting the caspase cascade

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20
Q

what are effector caspases responsible for

A

cleavage of cell substrates and mediate cell killing

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21
Q

what are caspases produced as

A

inactive zymogens

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22
Q

how are the inactive zymogens activated

A

they need to have 2 cleavages

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23
Q

what are the different inflammatory caspases

A

1,4,5,11,12,13 and 14

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24
Q

what are the different initiator capsases

A

2 and 9, 8 and 10

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25
Q

what are the different effector/ executioner caspases

A

3,6 and 7

26
Q

what happens to the initiator caspase as a result of the apototic signal

A

dimerization, activation and cleavage

27
Q

what does the active initiator caspase do

A

cleaves the executioner caspase

28
Q

what does the active executioner caspase do

A

cleaves multiple cell substrates to cause cell death (apoptosis)

29
Q

what do caspases do to cause cell death

A

they cleave structural proteins and DNA replication/repair enzymes

30
Q

what is ICAD

A

inhibitor of caspase-activated DNase

31
Q

normal function of PARP and consequence of inactivation

A

DNA repair, Disabled DNA repair

32
Q

normal function of DNA-RC and consequence of inactivation

A

DNA rep, halt DNA rep

33
Q

normal function of FAK and consequence of inactivation

A

regulate cell adhesion, cell detachment/migration

34
Q

normal function of NuMA and consequence of inactivation

A

nuclear integrity, nuclear disassembly

35
Q

normal function of α-fodrin and actin and consequence of inactivation

A

cytoskeleton, disassembly of cell structures

36
Q

what does intrinsic apoptosis cause

A

mitochondrial damage perturbation which causes cytochrome C release

37
Q

what happens in mitochondrial perturbation

A

the membrane changes and pores form, there is a loss of mitochondrial membrane potential that causes cytochrome C release

38
Q

what happens after Cytochrome C release in intrinsic apoptosis

A

the messenger binds to inactive APAF-1 and activates it which activates pro-caspase 9

39
Q

what is an apoptosome

A

an accumulation of APAF-1s

40
Q

What does the Bcl-2 family do

A

govern mitochondrial permeabilisation, they can promote or inhibit apoptosis

41
Q

what makes a protein part of the Bcl-2 family

A

all contain Bcl-2 homology domains , its not that they all have the same function

42
Q

2 different types of Bcl-2 proteins

A

Anti-apoptotic and pro-apoptotic

43
Q

anti-apoptosis Bcl-2 members

A

essential to life, if you get rid of them then cell populations reduce through apoptosis

44
Q

pro-apoptosis Bcl-2 members: effectors

A

form pores in mitochondria to release cytochrome C (BAK, BAX)

45
Q

pro-apoptosis Bcl-2 members: BH3

A

central to life and death decisions of the cell and activation during cell stress will dictate the outcome m

46
Q

when do cell surface receptors transmit a signal in extrinsic apoptosis

A

once the ligand has bound

46
Q

what happens when the ligand has bound in extrinsic apoptosis

A

the receptor recruits an adaptor protein which then activates a caspase resulting in a DISC

47
Q

what is a DISC

A

death inducing signalling complex

48
Q

in extrinsic apoptosis, what family are they receptors part of

A

Tumour necrosis factor receptor superfamily (TNFR)

49
Q

what does the TNFR superfamily include

A

TNFR, FAS receptor, TRAIL receptor 1&2

49
Q

what components are the TNFR receptors made of

A

it has a specific ligand, cytoplasmic region called a death domain (inside cell)

50
Q

what complicates death receptor mediated cell death

A

decoy receptors

50
Q

what supresses death receptor mediated cell death

A

FLIP

51
Q

overview of phagocytosis

A

phagocyte englufs particle for form phagosome for same packaging, anti-inflammatory allows adaptive immune responses to cell derived material, find me eat me signalling

52
Q

Evading apoptosis as a hallmark of cancer, why is it fundamental

A

cells dont die so they accumulate, they also fail to respond to treatment

53
Q

how cancer evades apoptosis - impaired receptor signalling pathway

A

reduced expression of death receptors, expression of decoy receptors (no death domain present) or death signals (ligands) so cell doesn’t get message to die

54
Q

how cancer evades apoptosis - disrupted balance of Bcl-2 family

A

overexpression of the anti-apoptotic proteins, underexpression of pro-apoptotic proteins (pores on membrane dont form)

55
Q

3 other ways that cancer evades apoptosis

A

reduced expression of caspases, increase expression of IAPs, defects/mutations in p53

56
Q

what does redundancy mean

A

theres multiple ways the cancer can take advantage of pathways e.g. in apoptosis, if one way doesn’t work it can do the others

57
Q

what happens with p53 loss

A

there is a reduction in apoptosis caused by cell stress or DNA damage

58
Q

how does p53 effect the Bcl-2 family

A

induces BH3-only proteins and allows function of effectors (Bax and Bak)

hallmarks of cancer (17 decks)

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