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Cancer Biology and Therapy > An emerging hallmark of cancer > Flashcards

An emerging hallmark of cancer Flashcards

1
Q

reprogramming of energy metabolism is classed as?

A

a new emerging hallmark of cancer

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2
Q

under oxygenated conditions how does cell metabolism work? be quite brief

A

under aerobic conditions, oxygenated non-malignant cells process glucose to pyruvate via glycolysis in the cytosol then to CO2 in the mitochondria

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3
Q

in anaerobic conditions, embryogenesis or exercise, what is the favoured metabolic pathway? how much pyruvate is used here?

A

glycolysis

relatively little pyruvate used

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4
Q

what is the Warburg effect?

A

cancer cells can reprogram glucose metabolism to predominantly glycolysis
regardless of oxygen availability

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5
Q

what is the product of glycolysis

A

lactate

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6
Q

how many ATP molecules are produced in oxidative phosphorylation compared to glycolysis?

A

op: 36 ATPs
glycolysis: 2 ATPS

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7
Q

how do cancer cells compensate for this decreased efficiency of glycolysis?

A

they compensate by upregulating glucose transporters

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8
Q

how can PET imaging be used to show where a cancer is?

A

can monitor glucose uptake

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9
Q

4 functional rational for the glycolytic switch?

A

rapid ATP synthesis
biosynthesis
tumour microenvironment
cell signalling

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10
Q
  1. Rapid ATP synthesis:

how much faster is glycolysis than op?

A

10-100 times faster

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11
Q
  1. Rapid ATP synthesis:

what advantage does a faster production of ATP provide tumour cells?

A

selective advantage when competing for shared and limited resources

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12
Q
  1. Rapid ATP synthesis:

can glycolysis produce as much ATP as respiration in the same time?

A

yes, occurs very rapidly and the cells are rapidly proliferating so their rate of metabolism is higher

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13
Q
  1. Rapid ATP synthesis:

why does the cancer cells want a selective advantage over other cells in the TME?

A

compete with cancer fighting cells

immune cells would need the same nutrient supply as tumour cells

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14
Q
  1. Biosynthesis:

explain why this is an advantage for cancer cells

A

glycolytic intermediates supply subsidiary anabolic pathways

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15
Q
  1. Biosynthesis:

example of a pathway glycolytic intermediates can supply

A

Pentose phosphate pathway

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16
Q
  1. Biosynthesis:

what des the pentose phosphate pathway support?

A

DNA and RNA replication

NADP production

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17
Q
  1. Tumour microenvironment:

how does the glycolytic switch help the TME?

A

decrease in pH due to lactate secretion which enhances invasiveness

increases NADPH and glutathione produced to counteract oxidative stress

successful seeding to organs may require low oxygen and nutrients so this prepares the cells for this

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18
Q
  1. Tumour microenvironment: what does lactate accumulation in the TME do? talk macrophages
A

suppress the anti cancer immune response by promoting M2 macrophage emergence= PROCARCINOGENIC

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19
Q
  1. Tumour microenvironment: M2 macrophages are good or bad for the tumour cells?
A

good

secrete high levels of pro carcinogenic cytokines

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20
Q
  1. Tumour microenvironment: what is the acid-mediated invasion hypothesis?
A

decreased pH due to lactate secretion enhances invasiveness

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21
Q

2 ways of cell signalling? (4th rational)

A

VIA ROS species

through chromatin remodelling

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22
Q

4a) Cell signalling through ROS:

effect of glycolysis on ROS? leads to?

A

produces it

cell signalling

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23
Q

4a) Cell signalling through ROS: how are ROS formed? examples of ROS?

A

reduction of O2

O2’, H202, OH’-

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24
Q

4a) Cell signalling through ROS: are ROS all toxic species?

A

no recently found that hydrogen peroxide can have a role as a 2ndary messenger which reversibly oxidises cystine In proteins to regulate response to metabolic stress

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25
Q

4a) Cell signalling through ROS: 2 ways of ROS production?

A

mitochondria complex I and II

NADPH oxidases (NOX) PPP

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26
Q

4a) Cell signalling through ROS: molecules leading to ROS elimination

A

glutathione peroxidase

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27
Q

4b) Cell signalling through chromatin remodelling: explain how glycolysis is linked to chromatin?

A

remodelling
lactate derived lactylation of histone lysine residues serves as an epigenetic modification which stimulates gene transcription for chromatin in macrophages

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28
Q

4b) Cell signalling through chromatin remodelling: which cells does chromatin get remodelled

A

macrophages

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29
Q

4b) Cell signalling through chromatin remodelling:

what happens to the macrophages after this change in DNA expression?

A

turn to inflammatory state

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30
Q

TF all tumours have the same pH levels. what does this suggest?

A

no they are all unique

suggests metabolic heterogeneity- multiple metabolic pathways used at once

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31
Q

TF: tumour cells only use glycolysis

A

no will also use respiration

glycolysis is the predominant pathway though

32
Q

TF OP and glycolysis aren’t competitive?

33
Q

what is metabolic symbiosis regarding OP and glycolysis?

A

seen in endometrial cancer
MCT1 seen more on the outer regions which are more oxygenated= respiration
MCT4 is more highly expressed towards the middle- less oxygen so glycolysis
= metabolic symbiosis

34
Q

tumour cells are _____ to glucose

35
Q

what is hif-1a? levels of it throughout cancer development

A

a transcription factor

levels stabilise as cancer progresses

36
Q

what must the cells gp through once they become hyper proliferative?

A

adaptive mechanisms to environmental and proliferative constraints such as lack of oxygen

37
Q

what seperates tumours from the stromal cells?

A

basement membrane

38
Q

centre of the tumour is _____ and has ____ oxygen supply

A

necrotic

no

39
Q

as a results of tumour cells having decreased oxygen what happens? explain

A

they become hypoxic

must either die to acquire a glycolytic phenotype to gain a survival advantage

40
Q

what does the transcription factor hif-1 actually do?

A

maintains glycolysis when the cells become hypoxic then stabilises

41
Q

what does the stabilisation of hif-1 do?

A

unregulated factors such as VEGF

42
Q

what is VEGF important in

A

angiogenesis

43
Q

Hif-1 affects which pathways? how

A

PI3K pathway by binding to RTKs on the cell surface

44
Q

in the tumour ME how do motile cells be produced? effect?

A

when it becomes more acidic it selects for motile cells. can now metastasis

45
Q

brief summary of environmental effects which lead to reprogramming of energy metabolism?

A

ME constraints

reduced oxygen levels and therefore HIF1a stabilisation and then the events after that

46
Q

HIF1a is a key regulator of ______ response. explain

A

glycolytic.

it mediates response to reduced oxygen levels

47
Q

levels of HIF1a ______ as cancer progresses. it responds to?

A

stabilise

low oxygen levels

48
Q

what can happen to HIF1a expression in cancers?

A

over expressed

49
Q

when oxygen is present what is HIF1a like?

A

HIF1a is hydroxylated in the presence of oxygen

binds to VHL which= ubiquitination which leads to proteasomal degradation

50
Q

what is HIF1a like in low oxygen conditions

A

decrease in HIF1a hydroxylation
stops binding to VHL
HIF1a can now form a heterodimer with HIF1b which can act as a transcription factor and activate genes for GF and angiogenesis

51
Q

when the HIF1a and HIF1B form a heterodimer due to low oxygen conditions, what can it do?

A

be a transcriptional factor and regulate genes for GF and angiogenic factors

52
Q

when the PI3K pathway is activated, what is activated downstream? effect of this on HIF?

A

AKT and mTor

activates HIF

53
Q

TF PI3K pathway doesn’t influence any transcription factors?

A

false
HIF1
FoxO
and SREBP

54
Q

HIF1 regulation via the PI3K pathway is oxygen _______

55
Q

FoxO is regulated by what?

56
Q

TF: AKT is one of the only regulators of FoxO function?

57
Q

effect of FoxO

A

regulate proliferation and metabolism

for insulin signalling- growth

58
Q

SREBP is regulated by?

59
Q

what is SREBP and what is it involved in?

A

transcription factor

involved in lipid homeostasis

60
Q

TF upregulation of PI3K can have a direct effect on glycolytic enzymes?

61
Q

What is the most important oncogene?

A

MYC oncogene

62
Q

what does the MYC oncogene control?

A

energy metabolism and proliferation

63
Q

what pathways does MYC expression activate?

64
Q

what enzymes does the MYC oncogene regulate?

A

glycolytic enzymes e.g. glucose transporters, hexokinases, amylase

65
Q

what pathway can MYC act via?

66
Q

which genes are MYC oncogenes related to

A

glycolytic genes

67
Q

how does MYC contribute to glucose and glutamine addiction in tumour cells

A

increases glutamine uptake

increase glucose transporters

68
Q

how can p53 effect metabolism?

A

expresses genes involved in glucose OP and lipid metabolism

69
Q

effect of p53 on glycolysis? how?

A

INHIBITS

by down regulating the glucose transporters which are the rate limiting transporters for glucose metabolism

70
Q

effect of p53 on TIGA? what does TIGA do?

A

induces tiga expression

Tiga indirectly inhibits 2 enzymes in glycolysis
diverts glycolytic intermediates into the PPP
G6PD leading to decreased NADP production

71
Q

p10 is a?

A

tumour suppressor

72
Q

how does p10 effect metabolism?

A

decreases glycolysis and promotes oxidative phosphorylation

73
Q

which glycolytic enzymes does p10 decrease levels of?

A

pyruvate kinase

phosphofructase

74
Q

effects of ROS on PI3K pathway?

A

potentiate activation of PI3K and AKT by inhibiting p10 our activating oncogenes

75
Q

effect of ROS on EGFR signally

A

unregulated

Cancer Biology and Therapy (23 decks)

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