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Y2 Cancer (MCD) > Invasion – Regulation of Cell Motility > Flashcards

Invasion – Regulation of Cell Motility Flashcards

1
Q

What are the changes that occur in the cells that occur during tumour progression?

A

Genetic alterations lead to hyperproliferation,

disassembly of cell-cell contacts,

loss of polarity,

increased motility

and cleavage of ECM proteins

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2
Q

What are the different types of tumour cell migration?

A

Single cell migration (ameboid)

Mesenchymal (single cells)

Mesenchymal (chains)

Clusters/cohorts

Multicellular strands/sheets

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3
Q

What physiological phenomena does tumour migration mimic?

A

Morphogenesis - the type of movement used by the cells during differentiation e.g. Branching morphogenesis, vascular sprouting etc.

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4
Q

What did a comparison of the expression profile of invasive cells vs primary tumours show to be upregulated in invasive cells?

A

Cytoskeleton regulation

Motility machinery

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5
Q

What makes normal migrating cells stop moving?

A

Contact inhibition of locomotion

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6
Q

How are tumour cells different in this aspect?

A

They lose contact inhibition of locomotion so they can multilayer

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7
Q

What is another term for ECM proteins?

A

Substratum

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8
Q

What are filopodia?

A

Finger-like protrusions that are rich in actin filaments

They sense the local environment

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9
Q

What are lamellipodia?

A

Sheet-like protrusions that are rich in actin filaments

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10
Q

What are the four main stages of cell movement?

A

Extension
Adhesion
Translocation
De-adhesion

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11
Q

What are the attachments between the cell and the surface that it is moving along called?

A

Focal adhesions

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12
Q

What are the monomers of actin filaments?

A

G-actin

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13
Q

Describe the polarity of acting filaments.

A

They have a plus end and a minus end

The monomers preferentially get added on at the plus end

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14
Q

What protein complex is important in initiating polymerisation?

A

Arp2 and Arp3

This forms a trimer with actin and is good at initiating polymerisation

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15
Q

What is the limiting step in actin dynamics?

A

Formation of Arp2/3-actin trimers to initiate polymerisation

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16
Q

State two proteins that bind to free G-actin and describe how they affect elongation.

A

Promote elongation = profilin (these deliver the G-actin to the growing filament)

Sequesters G-actin = beta–4 thymosin ADF, cofilin

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17
Q

Name some + end capping proteins.

A

CapZ
Gelsolin
Fragmin/severin

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18
Q

Name some – end capping proteins.

A

Tropomodulin

Arp2/3 complex

19
Q

Name some severing proteins.

A

Gelsolin ADF
Framin/severin
Cofilin

20
Q

What are the features of the actin filaments in severed populations?

A

Actin filaments can grow and shrink more rapidly

21
Q

What can happen to single filaments of actin to improve their structural integrity?

A

They can be bundled or cross-linked

22
Q

Name some proteins involved in cross-linking and bundling.

A 
Alpha-actinin 
Fimbrin 
Filamin 
Spectrin 
Villin 
Vinculin
23
Q

Which protein allows branching of the actin filaments?

A

Arp2/3 complex

24
Q

At what angle do they branch?

A

70 degrees

25
Q

Summarise the actions of Arp2/3 complex.

A

They initiate nucleation
They cap filaments
They cause branching

26
Q

Describe what causes the gel-sol transition.

A

The actin filaments can be severed to make the cell more fluid

27
Q

Describe the actin processes that take place during the protusion of lamellipodia.

A

There is polymerisation, disassembly, branching and capping

There is net filament assembly at the leading edge

28
Q

Describe the actin processes that take place during the formation of filopodia.

A

Actin polymerisation
Bundling and cross-linking
(NO branching)
As soon as the finger wants to retract it will collapse at the base

29
Q

State four signalling mechanisms that regulate the actin cytoskeleton.

A

Ion flux changes
Phosphoinositide signalling
Kinases/phosphatases
Small GTPases

30
Q

What are the three most important small GTPases in terms of the actin cytoskeleton and what does activation of each cause?

A

Cdc42 – filopodia
Rac – lamellipodia
Rho – stress fibres
NOTE: these are all part of the Rho family

31
Q

Explain how Rac causes actin polymerisation/organisation.

A

Rac binds to and activates WAVE

WAVE then activates Arp2/3, which is important in actin organisation

32
Q

Explain how Cdc42 causes actin polymerisation/organisation.

A

Cdc42 binds to WASP

WASP also activates Arp2/3

33
Q

Which small GTPases are involved in lamellipodia protrusion?

A

Rac

34
Q

Which small GTPases are involved in focal adhesion assembly?

A

Rac and Rho

35
Q

Which small GTPases are involved in contraction?

A

Rho (stress fibres are important for contraction)

36
Q

What cell machinery and migration strategies are used for INDIVIDUAL cell motility?

A

Strategies:
Ameoboid
Mesenchymal (single cells)

Machinery:
Integrins and proteases

37
Q

What cell machinery and migration strategies are used for COLLECTIVE cell motility?

A

Strategies:
Mesenchymal (chains)
Clusters/cohorts
Multicellular strands/sheets

Machinery:
Integrins, proteases, cadherins, gap junctions.

38
Q

During cell migration what does the leader cell(s) have to do?

A

Degrade the ECM in the path of the cell’s migration.

39
Q

What can stimulate a cell to move?

A

organogenesis and morphogenesis

wounding

growth factors
/chemoattractants

dedifferentiation (tumours)

40
Q

What are 2 types of motility?

A

Hapoptatic = random movement, not towards any particular location

Chemotactic = towards a very specific point

41
Q

What happens to actin filaments in a cell when a signal to move is received by the cell?

A

The filaments are dissassembled into their soluble monomers G-actin

This is then transported to the site of the signal and re-assembled

The cell can now contract on the side of the signal

42
Q

Where to focal adhesions form?

A

At the end of stress fibres where a cell is moving over a surface.

43
Q

What are the stages of actin dynamics?

A
  1. Nucleation
  2. Elongation
  3. Capping
  4. Severing
  5. Cross-linking
  6. Branching
44
Q

What is actin nucleation dependent on?

A

ATP

Y2 Cancer (MCD) (16 decks)

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