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Cancer Y2 > External Factors Affecting Cell Division and Tumour Growth > Flashcards

External Factors Affecting Cell Division and Tumour Growth Flashcards

1
Q

WHAT IS CELL BEHAVIOUR?

A

THE WAY CELLS INTERACT WITH EXTERNAL ENVIRONMENT AND THEIR REACTIONS TO THIS, PARTICULARLY PROLIFERATIVE AND MOTILE RESPONSES

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2
Q

WHAT EXTERNAL INFLUENCES ARE DETECTED BY CELLS? (2 types and a few examples)

A

CHEMICAL - Hormones, growth factors, ion concs, ECM, molecules on other cells, nutrients and dissolved gas concs
PHYSICAL - Mechanical stress, temperature, the topography (“layout”) of the ECM and other cells

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3
Q

WHAT EXTERNAL FACTORS CAN INFLUENCE CELL DIVISION?

A

 All external factors may influence cell proliferation, but the ones relating to cancer cell behaviour are:

  • Growth factors
  • Cell-cell adhesion
  • Cell-ECM adhesion
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4
Q

What happens if a cell hits a suitable culture surface

A
  • When a cell hits a suitable culture surface it spreads

- It then acquires a polarity and can become motile

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5
Q

Is cell spreading passive

A

No

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6
Q

Is cell spreading gravity-dependent

A

No

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7
Q

A suitable surface for a cell to adhere to is usually one that is coated with ….

A

an adhesive matrix molecule

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8
Q

What is more important than amount of space for cell spreading

A

distribution of the adhesion molecule

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9
Q

Example of an adhesion molecule?

A

Fibronectin

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10
Q

How do we know cells require to be attached to ECM (and able to spread) to begin protein synthesis and proliferation (DNA synthesis)

A

In suspension, cells don’t significantly synthesise protein or DNA

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11
Q

What is anchorage dependence

A
  • Attachment to ECM may be required for cell survival in most tissue cells
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12
Q

What cells do not have anchorage dependence

A

blood cells

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13
Q

How is there a Link between the cytoskeleton and the ECM

A
  • Cells have receptors on their cell surface which bind specifically to ECM molecules
  • These molecules are often linked, at their cytoplasmic domains, to the cytoskeleton
  • This arrangement means that there is mechanical continuity between ECM and cell interior
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14
Q

What protein is extremely important in cell-ECM adhesion

A

Integrins

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15
Q

Structure of integrin?

A

made of alpha and beta subunits which both span the membrane once
Matrix binding head, actin binding tail.

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16
Q

Formations of integrin? (3)

A

Knees flexed, extended legs open and extended legs closed

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17
Q

How many molecules can each integrin bind

A

 Some integrins only bind one particular molecule, others bind multiple

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18
Q

Examples of ECM molecules integrins bind to?

A

Collagens, laminin, fibronectin, fibrinogen

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19
Q

What links integrins to the actin cytoskeleton

A

Actin binding proteins

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20
Q
  • integrin complexes cluster to form….. (2)
A

focal adhesions or hemidesmosomes

21
Q

What other purpose to integrins serve other than cell adhesion

A
  • ECM receptors (e.g. integrins) can act to transduce signals
    the composition of the ECM will determine which integrin complexes bind and which signals it receives
    This can alter the phenotype of the cell
22
Q

The amount of force that is generated at a focal adhesion depends on both…

A

the force generated by the cytoskeleton (F cell) and the stiffness of the ECM

23
Q

Experiment that shows that the external environment affects the phenotype of the cell

A

One cell was mixed with type 1 collagen (interstitial matrix) and one with basal lamina matrix gel
In the collagen, the mammary epithelium did not differentiate into secretory cells
In the basal lamina matrix, the mammary cells organize into ‘organoids’ and produce milk proteins

24
Q

Example of inside out signalling?

A

. in inflammation or blood-clotting, switching on adhesion of circulating leukocytes

25
Q

Describe inside out signalling?

A
  • A signal from inside of the cell can act on the integrin complex and cause it to change from the low affinity bent closed legs complex to the high affinity complex straight open legs.
  • Inside-out signaling is where the activation of the complex causes a change in conformation to high affinity
26
Q

Describe outside in signalling?

A

ECM ligand binds causing further opening of the legs of the integrin, this exposes the binding site for recruitment of cytoplasmic signalling molecules

  • Outside-in signaling is where the ligand binds to this high affinity complex and causes the molecule to open up
27
Q

What is density dependence of cell division

A

when cell in culture form a confluent monolayer they stop proliferating and slow down many other metabolic activities.
It has also been shown that it is competition for external growth factors that does this and not cell cell contact.

28
Q

Similarity between Growth factor signals and integrin signals?

A

may actually stimulate similar, if not identical, signaling pathways
- Both of these signals are required to converge for proliferation to occur

29
Q

mechanism of anchorage depedence? (GF and integrin signalling)

A
  • Growth factor receptors and integrin signaling complexes can each activate identical signaling pathways (e.g. MAPK)
  • Individually, this activation is weak and/or transient
  • Together, activation is strong and sustained
  • the separate signaling pathways act SYNERGISTICALLY
30
Q

What are short tern contact interactions between cells

A

Transient interactions between cells which do not form stable cell-cell junctions

31
Q

What are long term contact interactions between cells

A

Stable interactions resulting in the formation of cell-cell junctions

32
Q

What is CONTACT INHIBITION OF LOCOMOTION

A

When most non-epithelial cells “collide”, they don’t form stable cell-cell contacts- they actually repel one another by paralyzing motility at the contact site, promoting the formation of a motile front at another site on the other cell, and moving off in the opposite direction

33
Q

what type of interaction generally happens between non-epithelial cells that collide

A

short term contact

34
Q

What cells tend to form long term contact when they collide

A

epithelial and endothelial cells

35
Q

What is contact induced spreading? What cells do this?

A

Contact between epithelial cells leads to the mutual induction of spreading, so that the total spread area of the contacted cells is greater than that of the sum of the two separated cells

36
Q

Epithelial cells require X in order to form junctions in many cases

A

calcium

37
Q

How does the formation of cell-cell junctions affect proliferation

A

reduces cell proliferation

38
Q

What state of activation is MAPK in and what is the level of p27 (cell cycle inhibitor) and level of proliferation in cells that have plentiful calcium

A

MAPK: low
p27: high
non-proliferating

39
Q

What state of activation is MAPK in and what is the level of p27 (cell cycle inhibitor) and level of proliferation in cells that have no calcium

A

MAPK: high
p27: low
proliferating

40
Q

What state of activation is MAPK in and what is the level of p27 (cell cycle inhibitor) and level of proliferation in cells that have cell cell junction

A

MAPK: low
p27: high
non-proliferating

41
Q

What state of activation is MAPK in and what is the level of p27 (cell cycle inhibitor) and level of proliferation in cells that have no cell cell junctions

A

MAPK: high
p27: low
proliferating

42
Q

Which is the master junction and what molecule does it contain

A

Adherens junctions and cadherin

43
Q

what is the relationship between beta catenin, cadherin, APC, and LEF1

A

The APC gene-product is a protein involved in the degradation of β-catenin. Β-catenin can also act as a transcription factor by teaming up with LEF-1 which is what happens when the APC complex is inactive. Beta-catenin is usually bound to cadherin at the membrane

44
Q

Mechanism of APC

A
  • Caused by a protein mutation in the beta-catenin molecule -> This molecule links the junction molecule to the cytoskeleton but also acts as a signaling molecule by binding with LEF-1 and entering the nucleus to cause gene transcription
  • Normally, beta-catenin is degraded in the cytoplasm, but in the case of APC it is not degraded as efficiently, so it builds up in the cytoplasm
  • This causes gene transcription (following association with LEF-1) which ultimately leads to proliferation
45
Q

Clustering of cadherins after cell-cell contact is known to alter the activation X e.g. Y is activated Z is inhibited; this can influence proliferation.

A 
X = Small GTPases
Y = Rac
Z = Rho
46
Q

Other than promoting the formation of solid tumours, what is an important consequence of loss of contact inhibition of locomotion for the progression of cancer?

A

Cancer is able to spread through many tissues because it loses contact inhibition of locomotion

47
Q

X is mutated in 30% of all cancers

A

Ras

48
Q

HOW DOES A PRIMARY CARCINOMA CELL METASTASISE? (4)

A
  • cell-cell adhesion must be down-regulated (e.g. cadherin levels reduced)
  • the cells must be motile
  • degradation of ECM must take place; matrix metalloproteinase (MMP) levels increased in order to migrate through basal lamina and interstitial ECM
  • the degree of carcinoma cell-cell adhesion is an indicator of how differentiated the primary tumour is, and indicates its invasiveness and the prognosis

Cancer Y2 (15 decks)

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