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Y2 MCD Cancer > carcinogenesis > Flashcards

carcinogenesis Flashcards

regulation of cell migration: explain the cytoskeletal processes occurring during locomotion, recall the types and roles of actin binding proteins, explain the role of second messengers as control mechanisms for cytoskeletal components, and explain the significance of metastasis in cancer development and the cellular and molecular changes necessary for it to occur

1
Q

4 molecular mechanisms that regulate motility in invasion

A

microfilaments, regulation of actin dynamics, cytoskeletal proteins, signalling proteins

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2
Q

structure of epithelium during homeostasis (become carcinoma)

A

epithelial cells (tightly cohesive cells, polarised, nucleus at base), basement membrane (“substratum”: support, protection), stroma

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3
Q

5 stages of tumour progression

A

homeostasis -> genetic alterations -> hyper-proliferation -> de-differentiation -> invasion

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4
Q

at what stage does a benign tumour form

A

hyper-proliferation (epipthelial cells in primary tumours are tightly bound together)

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5
Q

what 2 things happen in de-differentiation

A

disassembly of cell-cell contacts, loss of polarity

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6
Q

at what stage does a malignant tumour form

A

invasion

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7
Q

what 2 things happen in invasion

A

increased motility to break through basement membrane, cleavage of ECM proteins (find canals to migrate through dense stromal tissue into blood vessels)

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8
Q

what can cells do after metastising in blood stream

A

exit and invade a new organ, reacquiring new cell-cell contacts to form a new tumour

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9
Q

2 tumour cell migratory strategies

A

individual cells, collective cells

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10
Q

individual vs collective cell migration: metastatic potential

A

collective cells have higher metastatic potential than same number of individual cells

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11
Q

2 types of individual cell migration strategies

A

ameboid (round), mesenchymal (single cell)

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12
Q

tumour type of ameboid migration

A

lymphoma, leukaemia

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13
Q

tumour type of mesenchymal migration

A

fibrosarcoma, glioblastoma

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14
Q

3 types of collective cell migration strategies (must make more holes in stroma than individual cell migration)

A

mesenchymal (chain), cluster/cohorts, multicellular strands/sheets

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15
Q

tumour type of cluster/cohorts

A

epithelial cancer, melanoma

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16
Q

tumour type of mutlicellular strands/sheets

A

epithelial cancer, vascular tumours

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17
Q

2 key signalling molecules of individual cell migration

A

integrins (receptors regulating adhesion), proteases (digest basement membranes)

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18
Q

4 key signalling molecules of collective cell migration

A

integrins, proteases, cadherins (induce differentiation), gap junctions (collective signalling)

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19
Q

what cells direct invasion

A

tip cells

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20
Q

4 examples of morphological events which tumour cell metastasis mimics

A

2D sheets, branching morphogenesis (mammary gland), vascular sprouting, border cells (ovary)

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21
Q

features of tumour cell migration when empty space

A

invididual cells loosely packed, which when detect empty space migrate much faster than normal cells but in random directions and upon meeting other cells do not stop

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22
Q

with metastasising tumour cells, what genes are upregulated

A

cytoskeleton regulation, motility machinery

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23
Q

4 stimuli for cell movement

A

organogenesis and morphogenesis, wounding, growth factors / chemoattractants, de-differentiation (tumours)

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24
Q

in response to movement stimuli, what shape do cells change to

A

from round cells to cells with leading front and lagging back, becoming polarised (including organelle polarisation) in direction of motility

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25
Q

property that stops cells migrating

A

contact-inhibition motility by neighbour cells

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26
Q

what do cells have in order to move in response to stimuli

A

specialised structures (focal adhesion, lamellae, filopodium)

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27
Q

what 2 ECM proteins ensure cell remains attached to substratum

A

focal adhesions, filamentous actin

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28
Q

how does filamentous actin allow movement of cells

A

forms a hook on substratum, to provide traction forces for cell to move

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29
Q

2 features of integrin receptor

A

dimers of a and B subunits, with a very short tail

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30
Q

what forms on IC integrin receptor, and 2 functions

A

plaque of cytoskeletal proteins, allowing formation of signalling port and to connect with cytoskeleton

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31
Q

2 structures used for motility

A

fliopodia, lamellipodia

32
Q

what are filopodia

A

finger-like protrusions rich in actin filaments and vinculin (emerge at bottom of cell by basement membrane in migrating cells)

33
Q

what are lamellipodia

A

sheet-like projections rich in actin filaments (throw membrane to attach to basement membrane, move, then drawn back into cell to be thrown out again)

34
Q

where and why is control of cell movement needed

A

within a cell to coordinate what is happening in different parts, and outside a cell to respond to external influences (sensors, directionality)

35
Q

what is control of cell movement required for

A

regulating adhesion and release of cell ECM receptors (recycle adhesion molecules)

36
Q

2 types of cell motility

A

hapopatic (no-stimulus), chemotatic (stimulus)

37
Q

function of focal adhesion

A

connection to ECM

38
Q

4 stages of cell movement (cyclical)

A

extension -> adhesion -> translocation -> de-adhesion

39
Q

when cell extends (“steps”), what happens when lamellipodium lands on ECM

A

cell forms new focal adhesions to ensure connection to ECM

40
Q

what happens during translocation of cell

A

cell rear contracts, moving cell body forward

41
Q

what happens to old focal adhesion at rear

42
Q

2 forms of actin (polar and reversible, so can become each other)

A

monomer (G-actin; small soluble subunits), polymer (F-actin; large filamentous)

43
Q

upon EC signal for migration, what does IC actin do

A

disassembles all F-actin (filaments) -> actin subunits rapidly diffuse -> filaments reassemble at new site of EC signal for directionality

44
Q

what does actin form at location of new site

A

antiparallel contractile stress fibre cables (allow rear of cell to contract) with focal adhesions on end

45
Q

actin filament organisation from proximal to distal IC

A

stress fibres (antiparallel, with some having focal adhesions on end) -> lamellipodium (branches and cross-linked) -> filopodium (parallel) coming off at certain points

46
Q

2 G-actin remodelled filaments

A

sequestering (maintain G-actin soluble subunit pool), nucleating

47
Q

6 F-actin remodelled filaments

A

bundling, motor proteins, side-binding, capping, cross-linking, severing

48
Q

limiting step in actin dynamics (G-actin to F-actin)

A

nucleation

49
Q

nucleation process

A

to initiate polymerisation, actin monomers bind to Arp2 and Arp3, and then start forming filamentous actin trimers (minus end at ARP complex)

50
Q

what happens when initial F-actin produced

A

ARP complex detaches to allow elongation

51
Q

what allows elongation of F-actin

A

profilin, which forms a complex with an actin monomer and incorporates it into actin filament (cyclical)

52
Q

what blocks elongation of F-actin (promotes sequestering)

A

thymosin, which forms a complex with an actin monomer and prevents it binding to actin filament

53
Q

what other protein promotes G-protein sequestering, but does not inhibit polyermisation

A

ADF/cofilin

54
Q

process of capping

A

cap attaches to end of F-actin filament, preventing addition of more monomers

55
Q

capping proteins at + end of F-actin filament

A

cap Z, gelsolin, fragmin/severin

56
Q

capping proteins at - end of F-actin filament

A

tropomodulin, ARP complex

57
Q

process of severing

A

break up F-actin filaments but not always to monomeric forms, so that actin filaments grow and shrink more rapidly (unlike in unsevered, where growth and shrinkage is relatively slow)

58
Q

severing proteins

A

gelsolin, ADF/cofilin, fragmin/severin

59
Q

3 possible outcomes for actin function to generate filaments after severing

A

barbed (+) end capped before recycling its monomers to add to barbed-end of other segment via profilin, annealing (remending where severed) or growth from pre-existing end

60
Q

cross-linking and bundling mechanisms which shape and bundle filaments

A

fascin (parallel), fimbrin (parallel), a-actinin (parallel dimers), spectrin (star), filamin (cross-link at angles), dystrophin (link to plasma membrane)

61
Q

proteins involved in cross-linking and bundling

A

a-actinin, fimbrin, filamin, spectrin, villin, vinculin

62
Q

how can contracility of a F-filament be allowed using mysosin

A

myosin between 2 dimers form a buckle in one filament and a break above the buckle in another (by severin, ensuring same polarities face each other), so that the buckled filament can be contacted and extended (by sliding) in relation to the severed filament

63
Q

what is the branching protein of F-filaments, and at what angle does it do

A

ARP complex at 70 degrees (up to 3 binds when polymerising)

64
Q

describe gel-sol transition

A

gel (rigid) has many branches, but by severing proteins (e.g. gelsolin) being broken up to form severed filaments, it has same branches but filaments are broken up, meaning it is sol (can flow)

65
Q

diseases caused by deregulation of actin cytoskeleton

A

Wiskott-Aldrich syndrome (receptors can’t respond), Duchenne muscular dystrophy, Bullous pemphigoid (attachment proteins attacked by antibodies), Alzheimer’s (neurological); NOT hypertension (requires contraction of blood vessels, so functioning actin)

66
Q

what stage of cell movement does disassembly, nucleation, branching, severing, capping and bundling all occur in, and describe where these are happening

A

extension, when lamellipodium attempts to extend to next part of basement membrane (net filament assembly at leading edge, net filament disassembly behind leading edge to produce monomers to be brought to leading edge); same as in filopodia, where actin polymerises, bundles and cross-links at leading edge

67
Q

what stage of cell movement does gel/sol transition and attachment of ECM occur

A

adhesion, as upon binding F-actin can undergo gel-sol transition

68
Q

what stage of cell movement does contraction occur

A

translocation, with stress fibres contracting to pull rear of cell forwards

69
Q

what happens during de-attachement in filopodia

A

actin at leading edge is capped, before retrograde flow allows retraction and recycling of actin back into main cell body

70
Q

5 cell types with actin protrusions to support functional extensions

A

bristles, microvilli, stereocilia, filopodia, lamellipodia

71
Q

4 signalling mechanisms that regulate actin cytoskeleton

A

ion flux changes (e.g. IC Ca2+), phosphoinositide signalling, kinases/phosphatases, signalling cascades via small GTPases

72
Q

signalling cascades via small GTP proteins: how is Rho activated

A

GDP dissociates and GTP associates, causing response (upregulated in some tumours, whereas Ras is usually mutated)

73
Q

signalling cascades via small GTP proteins: what 3 things cause GDP to dissociate and GTP to bind

A

receptor tyrosine kinase, adhesion receptors and signal tranduction pathwyas

74
Q

signalling cascades via small GTP proteins: master regulator of flipodia

A

Cdc42 (polarises motility by sensing chemoattractants and actin polymerisation, preceeding Rac in lamellipodia)

75
Q

signalling cascades via small GTP proteins: master regulator of lamellipodia

A

Rac (in extension and focal adhesion phases of cell migration, and localised for direction)

76
Q

signalling cascades via small GTP proteins: master regulator of stress fibres

A

Rho (in focal adhesion, translocation (stress fibres, tension and contraction) and de-adhesion phases of cell migration, and localised for direction)

77
Q

signalling cascades via small GTP proteins: how to GTP proteins cause actin polymerisation and organisation

A

activate downstream pathways, including Pak, PI5K, formin and IQGAP, which activate different cascades (including Arp 2/3)

Y2 MCD Cancer (20 decks)

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