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Tumour Physiology > Metastasis-adhesion molecules > Flashcards

Metastasis-adhesion molecules Flashcards

1
Q

What is the go vs.grow hypothesis

A

That proliferation and cell migration are mutually exclusive.

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2
Q

What is intraversion and extraversion?

A

intraversion-it is the cells entering the blood stream

extraversion-cells entering the paranchymal tissue

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3
Q

What are the cell adhesison moleculeS?

A

dystroglycan
integrin
CD44
DDR

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4
Q

What are the characteristics of integrin?

A

Hetrodimer transmembrane
mg and calcium dependent
cystine flooded rich domain

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5
Q

What do the ecm-cell adhesion depend on? How about cell to cell adhesion?

A

fibronectin, laminin,collagen

V-CAM, ICAM, E-cadherin

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6
Q

What are the binding domains in the integrin? What are the ligands?

A

RGD-fibronectin

DGEA-collagen

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7
Q

What is the most optimal adhesion for migration?

A

Intermediate adhesion

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8
Q

FAK overexpression is associated with metastasis and i invasion

A

True

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9
Q

What is the role of FAC in cell migration?What signalling inhibits FAK?

A

It turnovers and remodels, it detaches from ECM to attach to it again to move, it does this by PDGF activating the pI3K pathway which inhibits FAC

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10
Q

What does the phosphorylation of src induce

A

metabolism, cytoskeletal changes

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11
Q

What proteins are involved in the migration of cells, forwar pseudopod formation and focal adhesion assembly? How does it do that?

A

rho,rac,cdc42.

It polymerizes actin and and creates stress fiber which allows it to move

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12
Q

What proteins are involved in focal adhesion disassembly? and how is done?

A

V-SRC is activated it will phosphorylate p190 which will increase p120(rho gtpase) prevents formation of stress fibre and new focal adhesion assembly.
Calpain woiuld cleave FAK which is an adaptor protein which is responsible for keeping FAC intact and mediates downstream signalling from src, integrin and growth factors, it will cause he disassembly of focal adhesion and impair src, integrin, growth factor signalling

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13
Q

What ‘s the role of ECM in metastatic cancer cells?

A

It provides structural support and biochemical signalling

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14
Q

What is the role of integrin in providing biochemical signallig to metastaic cells?

A

It can be inside out or outside in signalling through them respond to changes and can mediate changes

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15
Q

Overall what is the main steps that cells migrate? What is the importance of FAK

A

Cells have focal adhesion disassembly at the end but at the leading edge focal adhesion assembly at the leading edge, and FAK plays an important role in this procesS and upregulated in cancer

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16
Q

What signalling is involved in focal adhesion disassembly?

A

PDGF activates PI3K which activates PIP3 which dissociates the alpha and beta integrin which will then dissociate vinculin and a-actinin

17
Q

What part of the cell is calpain used?

A

The end of the cell

18
Q

What are the charecteristics of calpain? What is the difference between calpain 1,2, n-calpain? What protein regulates it’s actvity?

A

It’s intracellular cysteine rproteases, conserved non lysosomal, calcium dependent.
1,2-ubiquitously expressed
n-calpain- tissue specific
calpastatin

19
Q

What are the calpain substrates? What is it’s role in proliferation? What would counteract this effect?

A

Focal adhesion proteins, and cell cycle regulators such as p27,p53,cyclinD.
It promotes proliferation
Calpastatin

20
Q

What oncogene mediates calpain activity?

A

v-src

21
Q

How does increased EGF or any growth factor activity increase metastasis? specific mechanism

A

MAPK signalling pathway activated it can phosphorylate FAK which will mediate calpain activity and cleave FAK leading to the disassmebly of the FAC. the other indirect way is the dephosphorylation of FAK which will cause the disassmbly of FAC leading the cells to be detached from ECM leading to metastasis

22
Q

What are some integrins receptors that are overexpressed during metastasis? How are they related to metastasis

A

a6b1 and a6b4. They can be changed via inside out signalling of rho,growth factors, src, calpain

23
Q

How does a6b4 induce metastasis?

A

By being expressed in the leading edge and binding to actin instead of intermediate filament

24
Q

Where is a6b4 normally found and what does it bind to normally? what is it’s function normally?

A

It’s found in eoithelial cells binds to laminin and intermediate filament. cell adhesion

25
Q

How does DDR2 promote metastasis? Is DDR1 upregulated in breast, ovarian, pedriatic cancers?

A

By binding to collagen type 1 &3 and activating MMP which will degrade the matrix and promote invasion
yes

26
Q

What are the 3 different tissue invasions? And what are they characterized by?

A

collective multicellular intraversion- ECm remdelling
mesenchymal invasion-actin remodelling and protrusion
Both of these are proteolysis based
amoeboid invasion-Rock based cycles of contraction and expansion

27
Q

What are the differences between mesenchymal and amoeboid invasion?

A

1.rock independent but MMP, src,calpain,integrin dependeny
It has stronger matrix adhesion and more expression of a2b1 and ore autophosphorylation of FAK
While amoeboid has the opposite of those

28
Q

What does EMT transition depend on?

A

actin polymerization creating a protrusion

29
Q

What are the consequences of distrupting cell polarity? and what is cell polarity important for? How does it work

A

dysregulation of proliferation and apoptosis but it will promote invasion.
It’s important in downregulating signalling of the microenvironment
It works as adaptor and scaffolding proteins

30
Q

What are some potential therapeutic targets? What are the effects of these drugs on cells? What is an example of a drug that reduced invasion in anmal models?

A

MMP inhibitors, integrin inhibitors , growth factor inhibitors, src inhibitors
cytostatic
warfarin or sunitinib(non specific)

31
Q

How does tamoxifen work?

A

By acting on the e-cadherin and increasing cell cell adhesion

32
Q

Why is multi-agent therapy a good idea when treating cancer?

A

It’s able to treat the heterogenity of cancer, if you just treat the common subtypes of tumour population the uniques subpopulation will persist and colonize and take over

33
Q

Are there any ant-migratory drugs in clinical trials?

A

No

Tumour Physiology (11 decks)

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