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Biology of Disease > BOD L11+12 Cancer Signalling Networks > Flashcards

BOD L11+12 Cancer Signalling Networks Flashcards

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1
Q

What two things does interplay between tumour and ECM cause?

A

Increased cell prolifration.

Resistance to apoptosis

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2
Q

What are the three major kinds of cell death?

A

Apoptosis, necrosis, autophagy.

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3
Q

What role does autophagy play in cancer cell survival?

A

Cancer cells are able to upregulate autophagy to survive stress and increase growth.

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4
Q

What is the benefit of autophagy?

A

Provides fuel for energy/renewal of cell components during limited supply. Aids cell survival.

Conteracts consequences of aging by clearing damaged proteins.

Can also eliminate invading virus/bacteria.

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5
Q

How are genes involved in autophagy named?

A

AtgX (X being a number)

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6
Q

What two cell compartments are involved in autophagy?

A

Autophagosome and lysosomes.

Material and organelles are engulfed by the autophagosome and fuse with lysosomes for degradation (forms autolysosome)

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7
Q

How is autophagy triggered?

How does this tie in to tumour development?

A

Triggered by starvation and hypoxia.

In hyperplastic tumour, the core is hypoxic, so autophagy occuring here promoting cell survival

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8
Q

What protein is the cross-talker between autophagy and apoptosis?

A

Beclin-1

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9
Q

What does Beclin-1 interact with to inhibit autophagy?

A

Interacts with Bcl-2 and Bcl-XL (anti-apoptotic proteins).

Activation leads to inactivation of autophagy.

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10
Q

Many human cancers lose BECN1/ATG6 gene. What does this mean for beclin-1 and autophagy?

A

Beclin-1 may be tumour suppressive.

But cancers do need to autophage, and can increase this despite having lost this.

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11
Q

How can cancer cells increase autophagy with loss of ATG6/BECN1?

A

Supressing induction of p53,

maintaining metabolic function of mitochondria

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12
Q

What are membrane blebs a characteristic of a type of cell death?

A

Apoptosis

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13
Q

What is apoptosis?

A

Programmed cell death. Active, requires ATP

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14
Q

Cancer cells evade apoptotis, but how can apoptosis drive cancer growth?

A

After tissue injury, there is rapid regrowth of cells.

In tissues with pre-malignant cells, when growth signals are given to repair damage, these more aggressive cells will outgrow and cause development of early tumours.

Within tumours, apoptosis induced by chemo/radio induces death but leads to death-induced proliferation of surviving cells.

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15
Q

What are the hallmarks of apoptosis?

A

Cell shrinking and loss of cell contacts, and membrane blebbing is seen.

Inside the cell, chromatin condenses, nucleus fragments.

On the cell surface, lipids rearrange, with phosphatidylserine becoming exposed on the external leaflet of membrane.

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16
Q

How can apoptosis aid development?

A

Discarding of unneeded cells e.g. between fingers and toes

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17
Q

Through the various ways of inducing apoptosis, what single effectors play the essential role?

A

Caspases

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18
Q

How does caspase activation differ between intrinsic and extrinsic pathways?

A

Intrinsic, actiated by mitochondira (cytochrome C)

Extrinsic, activated by membrane death receptors

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19
Q

How many caspase genes are there, and what two kinds of caspases exist?

A

11 kinds caspase-1-to-10 and -14.

Initatiors and executioners.

Initiators activate executioners.

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20
Q

How do the two caspase proteins differ in their prodomains (distinguish between them)

A

Initiators have long prodomains, CARD or DED, whereas executioners have short.

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21
Q

Which are the executioner caspases?

A

3, 6 and 7 (14 found only in keratinocytes)

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22
Q

Which caspases are initiator caspases?

A

1, 2, 4, 5, 8, 9, 10.

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23
Q

Caspases can also be classified as pro- or anti- apoptotic.

Which are which?

A

Pro -

2,3,6,7,8.

Anti -

1,4,5

24
Q

Where do caspases target?

A

They target the c-terminal peptide bond side of an aspartate residue.

25
Q

How are caspases activated?

A

When activated, cleaved between p20 and p10 subunits.

These domains interact with one another to form active enzyme.

The enzyme consists of 2x large subunits (p20) and 2x small subunits (p10)

26
Q

What are IAPS?

A

inhibitos of apoptosis.

27
Q

What are some causes of intrinsic apoptosis?

A

DNA damage

cytoskeletal damage

ER stress

Loss of adhesion

Loss of growth factor

others…

28
Q

What is ER stress?

A

Build up of unfolded proteins. Halts ER function until resolved.

29
Q

How do the mitochondria sense the cells status?

A

Translocation of lipids from cell membrane, sense energy status/DNA damage/stress etc

30
Q

What is the normal role of cytochome C?

A

Transfers electrons as part of oxidative phosphorylation.

31
Q

What is the wheel of death?

A

Interaction of cytochrome C with Apaf-1, forming oligomer with caspase 9 in centre (active) forms apoptosome.

32
Q

Which caspase is active in the apoptosome?

A

Caspase 9, found in the middle of the apoptosome

33
Q

What are the targets of the apoptosome and thereby caspase 9?

A

Executioner caspases 3, 6 and 7 which cause apoptosis.

34
Q

What role does Bcl-2 play in cytochrome C release?

A

Bcl-2 controls release of mito proteins such as cytochrome C.

35
Q

Where is the Bcl-2 protein found?

A

Outer mitochondrial membrane.

36
Q

There are many family members in the Bcl 2 protein family. How do they direct apoptosis?

A

Some are pro-apoptotic and some are pro-apoptotic.

Influence keeping mitochondrial membrane channels open or closed.

37
Q

How do Bcl-2 and Bax family members counter one another in apoptosis?

A

Bcl-2 is anti-apoptotic.

Bax is pro-apoptotic.

38
Q

What role does BH3 protein play in Bcl-XL

A

Bcl-XL is anti-apoptotic, and inhibited by BH3 only protein binding.

39
Q

Many Bcl2 family members are active in the cell. How is apoptosis status determined?

A

Relative ratio (amounts) of Bcl2 and Bax proteins.

40
Q

What is MOMP and what is its role in apoptosis?

A

MOMP is mitochondrial outer membrane permeabilization.

Activity leads to commitment to apoptosis via release of intermembrane space proteins such as cytochrome C into cytoplasm.

41
Q

How can a Bcl2 family member be characterised as pro- or anti- apoptotic based on its domains?

A

If it has BH4 domain, anti-apoptotic.

If only BH3, pro-apoptotic

42
Q

How do mitochondria undergo MOMP?

A

Activated BAX insert in the OMM and form a pore to release cytochrome C.

These are activated by BH3-only proteins or p53.

But BCL2 can block this process.

43
Q

So what is the primary way that Bcl2 proteins influence apoptosis?

A

Opening/Closing of mitochondrial membrane channels (MOMP).

44
Q

What are the two ways apoptosis can be activated?

A

Cytochomre C release (activates caspase 9)

Smac/DIABLO release (inactivates IAPs) leads to liberation of caspases from IAPs

45
Q

What are three receptors that can initiate extrinsic apoptosis

A

Fas receptor (actv. by fas ligand)

TNF receptor (actv. by TNF ligand)

TRAIL receptor (actv. by TRAIL)

46
Q

How are Fas, TNF and TRAIL receptors also known?

A

Death receptors.

47
Q

How do Fas and TNF receptors induce apoptosis?

A

By promoting cytokines

48
Q

How do TRAIL receptors differ to TNF?

A

Subfamily of TNF receptor

TNF Related Apoptosis Inducing Ligand (TRAIL)

Similar to TNF, but only induce apoptosis in cancer cells.

49
Q

Which cells induce extrinsic apoptotic pathway?

A

CTLs and NK cells.

50
Q

How do killer cells induce apoptosis via extrinsic apoptotic pathway?

A

Release of granzyme B into cell (a protease)

Which is able to activate caspases.

51
Q

Which caspases does granzyme B cleave?

A

Executioner caspases 3 6 and 7

52
Q

Where do extrinsic and intrinsic apoptotic pathways converge?

A

At caspase 8 activation.

53
Q

What is necroptosis?

A

Programmed necrosis.

Occurs when apoptosis/caspases are blocked,

induced by the death receptors

54
Q

What is anoikis?

A

Apoptosis induced by loss of cell-matrix interactions.

Anoikis resistance is crucial for cancer metastasis

55
Q

What are the main ways that anoikis is evaded?

A
  1. EMT.
  2. Loss of epithelial characteristics (down reg of E-cadherin, upreg of N-cadherin).
  3. Alter cytoskeleton to promote migration, in search of new ECM.
  4. Inhibion of caspase-3
  5. Activation of pro-survival PI3K-Akt pathway

Biology of Disease (17 decks)

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