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Cancer Biology > Cell Death > Flashcards

Cell Death Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

What are the morphological characteristics of cell death?

A

Shrinkage
Membrane blebbing
Fragmentation
Nucleur condensation

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2
Q

How is apoptosis different from necrosis?

A

They are excreted so there is no inflammation

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3
Q

What gene is crucial for cell death in C.elegans?

A

CED3

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4
Q

Why is apotosis needed?

A

Proper embryonic development
For cells with sustained damage which cannot be repaired
Cells which have undergone senescence
It has outlived it’s usefulness
If it is required to maintain the normal physiological processes in an organism

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5
Q

How many cells die every second

A

One million cell die per second

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6
Q

Give 5 examples where apoptosis needs to occur to maintain the normal physiological processes of an organism

A

Shedding of the uterine lining
To remove mutations
The eye lens consists of apoptotic cells
Formation of the epidermis on the skin (protective dead skin layer)
Auto-reactive T cells which would kill healthy cells die before they reach the blood stream

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7
Q

What happens in Bax and Bak KO mice?

A

They cannot remove the skin between their paws

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8
Q

What happens to the brain of Caspase-9 KO mice?

A

They get an overgrowth of the brain

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9
Q

What is syndactyly?

A

Webbed feet and hands because the interdigital space fail to undergo apoptosis

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10
Q

What diseases are associated with too little apoptosis?

A

cancer
autoimmune diseases
viral infection

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11
Q

What diseases are associated with too much apoptosis?

A

Neurodegenerative diseases e.g. parkinsons
Viral infection e.g. HIV
Ischemic injury

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12
Q

What is ischemic injury?

A

Heart attack or strokes

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13
Q

How does apoptosis not induce inflammation?

A

The macrophages eat the dead cells

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14
Q

What are caspases?

A

Cysteine-dependent aspartate-directed phosphatases

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15
Q

Why are caspases so named?

A

The active site has a cysteine, which cleaves after aspartate residues

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16
Q

What are the two types of caspases?

A

Initiator

Executioner/ effector

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17
Q

What are the initiator caspases?

A

Caspases -8, -10, -9 and -2

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18
Q

What are the executioner caspases?

A

Caspase -3, -7 and -6

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19
Q

What is the function of initiator caspases?

A

They activate the executioner complexes through cleavage

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20
Q

What is the structure of initiator caspases?

A

they have a long prodomain that is important in their function

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21
Q

How are initiator caspases activated?

A

Autocatalytic processing triggered by co-factor binding and/ or oligomerisation

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22
Q

What is CAD?

A

caspase activated DNase

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23
Q

How does actin aid apoptosis induction?

A

cell rounding and shrinkage

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24
Q

How does acinus aid apoptosis induction?

A

Chromatin condensation

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25
Q

How does ICAD and PARP aid apoptosis induction?

A

DNA fragmentation

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26
Q

How does Gelsolin, ROCK-1 and PAK-2 aid apoptosis induction?

A

Membrane blebbing

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27
Q

How does Xkr8 aid apoptosis induction?

A

Externalisation of phosphatidyl serine on the plasma membrane

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28
Q

What is ICAD?

A

It is cleaved by caspases to activate CAD

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29
Q

What is CADs function?

A

Cleaves DNA between two nucleosomes

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30
Q

What is PARPs function?

A

Modifies histones by catalysing the formation of ADP-ribose and by binding to the DNA strands

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31
Q

How does CAD normally exist in a cell?

A

As an inactive complex with ICAD

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32
Q

What inhibits PARPs function to fix DNA damage?

A

cleavage by caspase 3

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33
Q

What is the function of lamins?

A

Maintain the shape of the nucleus

Mediate interactions between chromatin and the nuclear membrane

34
Q

What caspase degrades lamins?

A

Caspase 6

35
Q

What does lamin cleavage induce?

A

chromatin condensation and nuclear fragmentation

36
Q

What is the extrinsic apoptosis pathway?

A

Ligand binds to Death receptor -> FADD -> caspase 8 -> caspase-3 -> apoptosis

37
Q

What is the intrinsic apoptosis pathway?

A

Drug -> Cytochrome C -> Aparf-1 -> caspase-9 -> caspase-3 -> Apoptosis

38
Q

What does the ligand do to the death receptor?

A

Trimerisation and then polymerisation of the receptor

39
Q

Why is the death receptor altered?

A

To increase the affinity of FADD to the receptor

40
Q

What does FADD binding to the receptor cause?

A

Increased caspase-8 affinity to FADD

41
Q

What ligand binds to the death receptor?

A

FAS

42
Q

How is cytochrome C released?

A

By mitochondria using ATP

43
Q

What does cytochrome C binding to aparf1 do?

A

Changes the shape to adapt to a quaternary structure

44
Q

What does aparf1 binding to caspase-9 cause?

A

Apoptosome formation

45
Q

What is the apoptosome?

A

7 components of aparf-1, caspase-9 and cytochrome c

46
Q

What is the activation platform for caspase8 called?

A

death-inducing signalling complex (DISC)

47
Q

What is DISC?

A

The death receptor and FADD

48
Q

What is FADD?

A

An adaptor protein

49
Q

What is the function of caspase-9?

A

To convert pro-caspase-3 to caspase-3

50
Q

How does cytochrome C leave the mitochondria?

A

Through apoptosis-inducing signals which cause mitochondrial outer membrane permeabilisation and therefore cytochrome C can exit

51
Q

What is BCL-2?

A

A pro-survival signal

52
Q

What are BAK and BAX?

A

Pro-apoptotic signals

53
Q

What is BCL-2 function?

A

To inhibit cytochrome C release by inhibiting Bax

54
Q

what is Bax/Bak function?

A

to stimulate cytochrome C release

55
Q

What is BID, BIM and BAD?

A

BH3-only proteins

56
Q

What is the difference between Bcl-2 anti-apoptotic and pro-apoptotic proteins?

A

Pro-apoptotic proteins do not have a BH4 domain

57
Q

What is the function of BAD?

A

Binds to Bcl-2 to inhibit the oligomerisation of Bcl-2

58
Q

What is the function of BIM?

A

Too bind to BAX and inhibit oligomerisation of Bcl-2

59
Q

How do Bax and Bak directly permeabilise the mitochondrial outer membrane?

A

They oligomerise -> make MOMP -> form proteinaceous chanels and lipid pores for cytochrome C to move through

60
Q

What happens in B cell lymphoma?

A

BCL-2 of chromosome 18 translocates onto chromosome 14

This enhances BCL-2 function

61
Q

What is the function of Myc?

A

To increase proliferation and cause apoptosis

62
Q

How do survival factors interact with Myc?

A

They inhibit their ability to cause apoptosis

63
Q

What effect does the removal of p53 cause?

A

Inhibition of all apoptotic pathways since it controls the extrinsic and intrinsic pathway

64
Q

As well as keeping cells alive, how else does apoptosis effect cancer cells?

A

Allows them to live in hypoxic and nutrient poor environments
Promote metastasis

65
Q

What is anoikis?

A

when our cells in the body detach from membranes and other cells to undergo apoptosis

66
Q

What mechanisms do cancer cells induce to avoid apoptosis?

A

Mutation in death ligands or receptors
some mutations of TP53
Expression of ‘decoy’ TRAIL receptors
Loss of caspases
Loss of pro-apoptotic Bcl-2 family members
Upregulation of IAPs
Upregulation of anti-apoptotic Bcl-2 family members

67
Q

What are IAPs?

A

small proteins in the mitochondria

68
Q

How can anti-apoptotic genes be altered?

A

Gene translocation
Amplification
Overexpression

69
Q

How can pro-apoptotic genes be altered?

A

Genomic loss
Silencing
Mutation

70
Q

Describe fragment based drug design

A

Identify chemical fragments that bind the protein of interest by NMR -> Low affinity -> Connect fragments together -> High affinity fragment -> drug

71
Q

Name a BH3-mimic compound

A

Navitoclax

72
Q

What is Navitoclax commonly used for?

A

Leukaemia to sensitise cells to apoptosis

73
Q

Why isn’t navitoclax used as openly anymore?

A

Due to off target toxicities

74
Q

How does navitoclax work?

A

Target platelets and stop the differentiation of cells and cause them to die
inhibits BCL-xL, Bcl-W and Bcl-2

75
Q

What can venetoclax be used in combination for?

A

Increase BCL-2 priming
Target resistance factors
Mobilise tumour cells

76
Q

How can venetoclax be used in combination to increase BCL-2 priming?

A

Add a priming agent, e.g. PI3Kdelta inhibitors, to BCL2 -> BCL-2 to bind to BIM -> Add venetoclax and BIM will bind to BAX and BAK -> Apoptosis

77
Q

How can venetoclax be used in combination to target resistance factors?

A

Venetoclax will inhibit BCL-2
Add another agent e.g. JAK2 inhibitor, to block another anti-apoptotic enzyme
-> Apoptosis

78
Q

How can venetoclax be used in combination to mobilise tumour cells?

A

Add an mobilising agent, e.g. PI3Kdelta, to peripheral blood -> add venetoclax -> apoptosis

79
Q

What is BH3 profiling?

A

Testing to see if patients cancer cells are ‘primed to die’ and therefore they will respond to drugs which induce mitochondrial apoptosis

80
Q

How do you compete BH3 profiling?

A

Add BH3 peptide to cells, the more sensitive they are, the more primed to die they are
Liquid or solid tumour sample -> single cancer cell suspension -> exposure to treatments -> Permeabilisation, staining and peptide exposure -> Analysis -> results

81
Q

In terms of leukaemia, what do you measure when doing a BH3 profile?

A

The level of apoptosis and the release of cytochrome C

Cancer Biology (13 decks)

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