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MCD > Cancer 9: External factors controlling division > Flashcards

Cancer 9: External factors controlling division Flashcards

1
Q

What are the two types of external influences detected by cells?

A
  • chemical

- physical

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2
Q

Give examples of chemical influences

A

hormones, growth factors, ion concs

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3
Q

Give examples of physical influences

A

mechanical stresses, temperature

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4
Q

What external factors INFLUENCE cell division?

A
  • growth factors
  • cell-cell adhesion
  • cell-ECM adhesion
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5
Q

Why does cell spreading require energy?

A

-modulate cell adhesion and the cytoskeleton

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6
Q

How does cell-ECM adhesion influence cell proliferation?

A

-cells need to be bound to extracellular matrix to be fully competent for responding to soluble growth factors

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7
Q

What processes can occur ONLY when the cell is attached to ECM

A
  • protein synthesis and proliferation

- attachment to ECM may be required for cell survival

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8
Q

What determines the cell phenotype and give examples

A

-the composition of the matrix

in interstitial matrix - mammary epithelium does not differentiate to secretory cells
in basal lamina matrix - mammary cells organise into organoids and produce milk proteins

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9
Q

How does the cell receive information about its surroundings from ECM adhesion?

A
  • cells have receptors on their surface that 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 the cell interior
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10
Q

What is the structure of integrins?

A
  • heterodimer complexes of alpha and beta subunits
  • associate externally by their head regions
  • the leg regions span the plasma membrane

-ligand binding occurs at the junction of the head region

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11
Q

How do most integrins link to the actin cytoskeleton?

A

-via actin-binding proteins

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12
Q

What do integrin clusters form?

A
  • focal adhesions or hemidesmosomes
  • these clusters are involved in signal transduction

-some integrins also bind to specific adhesion molecules on other cells

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13
Q

How is signalling via ECM receptors carried out?

A

they can transduce signals

ECM binding to an integrin complex can stimulate the complex to produce a signal inside the cell

OUTSIDE- IN INTEGRIN SIGNALLING

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14
Q

How can cell-ECM adhesions and signals be turned off and on?

A

-conformational changes of the integrin complex to adopt flexed and extended molecular confirmations

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15
Q

What does the mechanical force produced depend on?

A
  • the force generated by the cytoskeleton
  • the stiffness of the ECM

-focal adhesions sense the mechanical properties of their surroundings

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16
Q

What to integrins recruit and to do what?

A

-cytoplasmic proteins which promote both signalling and actin assembly

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17
Q

What is INSIDE-OUT integrin signalling?

A

-a signal generated inside the cell can act on an integrin complex to alter the affinity of an integrin

18
Q

Give an example of inside-out integrin signalling

A

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

19
Q

What is the position of the integrin for low-affinity and high-affinity?

A

low affinity: bent confirmation, weak or no binding to ligand

high affinity: extended confirmation, strong binding to ligand

20
Q

What happens to the structure of the integrin when ECM binds to it?

A
  • it causes further opening of the legs which exposes the binding sites for the recruitment of cytoplasmic signalling molecules
21
Q

What do cells compete for at high density?

A

growth factors

22
Q

What are the steps of the ERK MAP kinase cascade?

A

growth factor binds to receptor and activates ras - raf-MEK-ERK
-this leads to gene expression and proliferation

23
Q

Why is proliferation dependant on anchorage?

A
  • growth factor receptors and integrin signalling complexes activate identical signalling pathways but are weak individually
  • however together activation is strong and sustained
24
Q

What is the difference between cell junctions of short and long term contact interactions?

A

SHORT TERM: do not form stable cell-cell junctions

LONG TERM: formation of cell-cell junctions

25
Q

What happens when most non-epithelial cells collide?

A

they repel each other by paralysing ,motility at the contact site
this promotes the formation of a motile front at another site of the cell so it moves in a different direction

-CONTACT INHIBITION OF LOCOMOTION

26
Q

Which types of cells strongly adhere to form specific cell-cell junctions?

A
  • epithelial cells
  • endothelial cells
  • neurones
27
Q

What two ways are junctions usually arranged as?

A
  • continuous belts (zonula)

- discrete spots (macula)

28
Q

What does contact between epithelial cells induce?

A

-mutual induction of spreading so that the total spread area is larger than the area of the 2 cells individualy

29
Q

How does calcium effect cell proliferation?

A
  • decreased calcium leads to high proliferation as it promotes no cell-cell junctions, activated MAPK
  • increased calcium leads to promotion of cell cell junctions, inactive MAPK and low proliferation
30
Q

How does adhesion blocking antibody effect proliferation?

A
  • increased antibody promote no cell-cell junctions, activated MAPK and high proliferation
  • decreased antibodys promotes cell-cell junction formation, inactive MAPK and low proliferation
31
Q

What is the adherens junction comprised of?

A

cadherin
beta catenin
alpha catenin
actin filament

32
Q

What is the adenomatous polyposis coli gene-product?

A
  • protein involved in the degradation of the junction-associated molecule, beta catenin
33
Q

How can B-catenin lead to cell proliferation?

A

beta catenin binds to LEF-1 to form a complex that enters the nucleus and influences gene expression, leading to proliferation

34
Q

How does clustering of cadherins effect proliferation?

A

clustering after cell-cell contact is known to alter the activation of small GTPases

some growth factor receptors are associated with cell-cell junctions- reducing their capacity to promote proliferation

35
Q

What can happen when cells lose their social skills?

A
  • proliferate uncontrollably
  • less adherent and will multilayer
  • epithelia breakdown cell-cell contacts
  • express telomerase
36
Q

What is the definition of an oncogene?

A

-mutant gene which promotes uncontrolled cell proliferation

37
Q

What is the definition of a proto-oncogene?

A

-normal cellular gene corresponding to the oncogene

38
Q

What occurs with uncontrolled proliferation of tissue cells?

A

mutant genes and constantly active products mean that neither growth factor or ECM signals are required to simulate proliferation

39
Q

What is a major feature of cancerous tumours?

A
  • their ability to spread

- deregulated proliferation

40
Q

How does a primary carcinoma cell metastasise?

A
  • cell-cell adhesion must be down regulated
  • cells must be motile
  • degradation of ECM must take place

NB the degree of carcinoma cell-cell adhesion is an indicator of how differentiated the primary tumour is, its invasiveness and the prognosis

MCD (13 decks)

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