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Year 2 Collin > Cancer 7 - External Factors controlling division and behaviour of normal and cancerous cells > Flashcards

Cancer 7 - External Factors controlling division and behaviour of normal and cancerous cells Flashcards

1
Q

What is cell behaviour

A

The way cells interact with external environment and their reactions to this - especially proliferative/motile responses

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2
Q

Which 3 factors contribute largely to cell proliferation

A
  1. GFs
  2. Cell-cell adhesion
  3. Cell-ECM adhesion
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3
Q

Cells often obtain polarity on ECM. Which part is usually the motile part?

A

The front part - contains lamellipod

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4
Q

Cell spreading is not a gravity-dependent event. What prerequisite is needed for cell spreading?

A

Energy

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5
Q

Cells need to be bound to ECM for?

A

In order to be fully competent to respond to soluble GFs - higher probability of entering S phase if they are able to spread more

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6
Q

Do cells significantly synthesise protein or DNA in suspension (i.e. not attached to ECM or spread)

A

No - attachment to ECM may be crucial for cell survival - “Anchorage dependance”

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7
Q

Cell phenotype can be determined by ECM composition. Give an example

A

Cultured mammary epithelium - in:
1. Interstitial matrix (type 1 collagen) - no differentiation to secretory cells

  1. Basal lamina matrix (basement membrane) - mammary cells become “organoids” and produce milk proteins
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8
Q

Cells have receptors that bind to ECM - give an example

A

Integrins

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9
Q

Integrins are heterodimer complexes. What are their subunits and describe them

A

alpha subunit - consists of 2 parts with a disulphide bridge

beta subunit - 1 long chain with cysteine-rich domains

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10
Q

Integrin complexes - which part associates with the extracellular region?

A

The “head” regions.

the leg regions span the plasma membrane

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11
Q

Where does ligand binding occur in an integrin complex

A

At the junction of head regions

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12
Q

On integrins, what does the a5B1 fibronectin receptor bind to?

A

Arg-Gly-Asp (RGD)

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13
Q

Not all integrins bind to matrix - what else may integrins bind to?

Give an example

A

May also bind to specific adhesion molecules on other cells

e.g. ICAM-1 on endothelial cells in inflammation

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14
Q

What do most integrins link to within the cell

A

Actin cytoskeleton via actin binding protein

Exception = a6b4 integrin - found in epithelial hemidesmosomes - linked to cytokeratin (intermediate filament network)

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15
Q

Integrin complexes cluster. What may they form

A
  1. Focal adhesions (most)

2. Hemidesmosomes (a6b4)

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16
Q

Integrins can act as signal transducters. What 2 forms can this take?

A

“Outside-in” integrin signalling / “Inside out”

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17
Q

Describe how outside in signalling works

A
  1. ECM composition determines which integrin complexes binds
  2. Upon binding - ECM composition determines which signals cells receive

This can alter cell phenotype

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18
Q

What factors can determine the force generated at a focal adhesion point

A
  1. Force generated by cytoskeleton

2. ECM stiffness

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19
Q

Integrins recruit cytoplasmic proteins for 2 functions. What are the 2 functions

A
  1. Promote signalling

2. Promote actin assembly

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20
Q

“Flexed/bent” integrins are?

A

Inactive - i.e. dont bind to ligands, low affinity

21
Q

Blood clotting and inflammation are examples of what type of signalling

A

“Inside out signalling”

22
Q

How does inside out signalling work

A

Signal generated inside cell (e.g. through hormone binding on receptor) - causes integrin complex to alter its affinity for ECM binding

23
Q

The extended conformation is?

A

High affinity for ECM

24
Q

How can low affinity integrin become high affinity integrin

A

Signal from inside the cell acts on integrin complex - inside out activation

25
Q

Once integrin binds to ECM, there is further opening (extension) of the legs of integrin. Why

A

Exposes sites of binding for cytoplasmic signalling molecules - outside-in activation

26
Q

What is meant by density-dependance of cell division

A

Higher the density of cell division - the less proliferation there is (due to competition for GFs)

27
Q

Which 2 signals are needed for efficient stimulation of proliferation?

A
  1. Gf

2. ECM

28
Q

Why do GF receptors and integrin signalling complexes activate identical signalling pathways (e.g. MAPK)

A

Because individually, the activations are weak but together they are strong and sustained - hence why both pathways act synergistically

29
Q

Describe the 2 types of contact interactions between cells and their nature

A

Short term - transient interactions between cells - don’t form stable cell-cell junctions

Long term - stable interactions resulting in cell-cell junction formation

30
Q

How do cells ensure that they do not multilayer in culture and in vivo

A

“Contact inhibition of locomotion”

When 2 non-epithelial cells collide - they repel one another by paralysing motility at the contact site, and form motile front at a different site in the cell and move off

31
Q

Name some cells that form long term cell-cell contacts

A

Epithelial cells
Endothelial cells
Neurones forming synapses

32
Q

How can contact between epithelial cells result in a stable monolayer?

A

When 2 epithelial cells contact - there is a mutual induction of spreading - total spread area > 2xindividual spread area (if they were separate)

33
Q

Which ion influences the formation of cell-cell junctions

A

Ca2+

34
Q

How may the formation of cell-cell adhesion reduce cell proliferation

(in some cell types)

A
  1. Cell-cell junctions form
  2. MAPK inactive
  3. Increased p27KIP1 (inhibitor of proliferation)
  4. Less/low proliferation
35
Q

What are cadherins associated to?

A

Cadherins are cell adhesion molecules - they are associated with B-catenin and a-catenin

36
Q

In APC (colon) - what protein is involved

A

Protein involved in degradation of b-catenin (which is associated with cell-cell junctions)

(Not enough protein made)

37
Q

B-catenin can also act as a transcription factor when associated with?

A

LEF-1

38
Q

How does the APC complex influence the cells actions

Usually APC active, if not APC happens in colon

A

IF APC ACTIVE: rapid degradation of b-catenin

IF APC INACTIVE - b-catenin associates with LEF-1 and acts as. TF stimulating cell proliferation

39
Q

Clustering of cadherins after cell cell contact can alter GTPase activation. What consequence does this have

A

Rac activated, Rho inhibited - influences proliferation

40
Q

Some GF receptors are associated with cell cell junctions - What does this mean

A

Reduced capacity to promote proliferation

41
Q

What may cause a cell to proliferate uncontrollably?

A

Lost density dependence of proliferation

42
Q

What may cause cells to be less adherent and multilayer

A

Lost contact inhibition of locomotion and anchorage dependance

43
Q

When can cancer occur

A

if cells:

  1. Proliferate uncontrollably
  2. Less adherent - multilayer
  3. Epithelia breakdown cell cell contacts
  4. Not hay flick limited - express telomerase - immortalised
44
Q

What may add to the invasive property of cancerous tumours?

A

Loss of contact inhibition of locomotion

45
Q

Ras is mutated in approximately what percentage of cancers

A

30%

46
Q

Most adult cancers are cancers of?

A

Epithelia - i.e. carcinomas

47
Q

What does the degree of carcinoma cell-cell adhesion indicate?

A
  1. How differentiated primary tumour is

2. Invasiveness and prognosis

48
Q

What are 3 requirements for metastasis

A
  1. Cell-cell adhesion downregulation
  2. Cells must be motile
  3. ECM degradation - e.g. through MMPs

Year 2 Collin (114 decks)

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