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Cancer Lectures > Epithelial-Mesenchymal Transition > Flashcards

Epithelial-Mesenchymal Transition Flashcards

1
Q

How are epithelial cells linked to each other?

A

Tightly

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2
Q

Where is the junctional complex of epithelial cells located?

A

At the most apical part of the lateral membrane

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3
Q

What three components does the junctional complex of epithelial cells consist of?

A

Tight junctions, desmosomes and adherens junctions

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4
Q

List the components found in adherens junctions

A 
F-actin
Alpha- and beta-catenin
E-cadherin
p120ctn
Vinculin
Alpha-actinin
VASP
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5
Q

Give an example of a transcriptional regulator involved in tight junctions

A

ZONAB

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6
Q

Give an example of a regulatory protein involved in tight junctions

A

G proteins

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7
Q

What is the main component found in tight junctions?

A

Actin filaments

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8
Q

Give an example of an adaptor protein involved in tight junctions

A

ZO-1

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9
Q

Give an example of a transmembrane protein involved in tight junctions

A

Occludin

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10
Q

What is the function of tight junctions?

A

To act as a barrier/fence

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11
Q

List the components found in desmosomes

A 
Desmoplakin
Desmoglein
Desmocolin
Plakophilin
Plakoglobin
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12
Q

What makes up a desmosomal complex?

A

Desmoglein/desmocolin-plakoglobin-desmoplakin-filaments (intermediate)

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13
Q

What is EMT characterised by?

A

Loss of cell adhesion
Repression of E-cadherin expression
Increased cell motility

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14
Q

What are the changes that occur for epithelial cells to transition into mesenchymal cells?

A

Changes in gene regulation, cell adhesion and cytoskeletal organisation
Reduction in E-cadherin or increased vimentin

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15
Q

EMT is an irreversible process, true or false?

A

False, EMT is reversible

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16
Q

Where are EMT and MET often observed in normal human cells?

A

During embryonic development

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17
Q

At what stage in the linear tumour progression model is EMT observed?

A

In the change from a carcinoma to a metastatic tumour

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18
Q

Who came up with the theory of parallel progression of primary and secondary tumours?

A

Christoph Klein

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19
Q

What are the transcription factors that control EMT in embryonic development?

A 
SNAIL
SLUG
ZEB1
ZEB2
TWIST1/2
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20
Q

What does SNAIL (SNAIL1) play a role in?

A

Gastrulation

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21
Q

What does SLUG (SNAIL2) play a role in?

A

Melanocytic lineage

Hematopoietic stem cells

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22
Q

What does ZEB2 (SIP1) play a role in?

A

Neural crest formation

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23
Q

What does ZEB1 (DeltaEF1) play a role in?

A

Bones and thymic T-cell development

24
Q

What does TWIST1 play a role in?

A

Neural tube defects

25
Q

How do the sizes of EMT transcription factors vary?

A

Between ~160 amino acids to ~1200 amino acids

26
Q

List some domains commonly found in EMT transcription factors

A 
CtBP binding site
Zinc finger
Homeodomain
SNAG domain
Serine-rich domain
Nuclear export sequence
Basic domain
HLH domain
Slug domain
Twist box
27
Q

What does ZEB2 induce in A431 cells and what is the affects of the zinc finger mutant?

A

Induces genetic reprogramming

Zinc finger mutant does not affect gene expression

28
Q

What is a microRNA and what is it implicated in?

A

22 nt non-coding RNA species implicated in posttranscriptional regulation of gene expression
Binds to mRNA to stop translation or cause degradation of the mRNA

29
Q

What microRNA family is ZEB1/2 expression regulated by?

A

miR-200

30
Q

What microRNA is SNAIL expression regulated by?

A

miR-34

31
Q

What do miR-200 and miR-34 link EMT with?

A

p53

32
Q

Finish this sentence, p53 is a guardian of epithelial…

A

Identity

33
Q

Give some properties of epithelial cells

A

Cell to cell adhesion
Low motility
E-cadherin/catenin

34
Q

Do the same or different signalling pathways induce EMT transcription factors?

A

Different

35
Q

Give some properties of mesenchymal cells

A

Cell-matrix interaction
High motility
N-cadherin/vimentin
MMPs/collagen

36
Q

What does TGFbeta regulate?

A

The ZEB/miR-200 network

37
Q

What are the phases of the cell cylce?

A

(G0), G1, S, G2, M

38
Q

How does the DNA content change during S phase?

A

Increases progressively from 2N to 4N

39
Q

What is the DNA content during G2 and M phase?

A

4N

40
Q

How does mitosis affect the DNA content?

A

Allows the return to the normal 2N value for phases G0 or G1

41
Q

What do the checkpoint controls check?

A

Am I OK to proliferate?
Is the previous phase completed?
Is this timely?
Is my DNA damaged?

42
Q

Name a key protein involved in cell-cycle progression

A

Retinoblastoma protein

43
Q

What transcription factor arrests cells in G1 phase?

A

ZEB2

44
Q

How does ZEB2 arrest cells in G1?

A

By transcriptional repression of cyclin D1

45
Q

Describe the correlation between cyclin D1 and ZEB2?

A

Inverse

46
Q

What does SNAIL do in MDCK cells?

A

Downregulates D cyclins

Induces G1 cell cycle arrest

47
Q

Give an example of an E-cadherin dominant negative mutant

A

EcWVM

48
Q

G1-S transition is not affected in EMT induced by a dominant negative E-cadherin, true or false?

A

True

49
Q

How do conventional cancer therapies work?

A

They induce DNA damage (via ATM or ATR)

50
Q

What does ZEB2 delay in RT112 cells?

A

UV- and cisplatin-induced apoptosis

51
Q

Response to radiotherapy in bladder cancer patients depends on the status of what transcription factor?

A

ZEB2

52
Q

What are EMT-inducing transcription factors otherwise known as?

A

Oncogenes

53
Q

What does TWIST1 facilitate the escape from?

A

Oncogene-induced senescence and apoptosis

54
Q

What do EMT-inducing transcription factors block?

A

Oncogene-induced senescence

55
Q

What cells do EMT programs generate which is in accordance with the definition of ‘cancer stem cells’?

A

More tumourigenic (escape anti-oncogenic barrier of premature senescence)
Slowly proliferating
Drug resistant

56
Q

Master regulators of EMT control diverse cancer-related pathways, true or false?

A

True

Cancer Lectures (24 decks)

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