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CAN > L17: Reprogramming Energy Metabolism In Cancer > Flashcards

L17: Reprogramming Energy Metabolism In Cancer Flashcards

1
Q

What are the 6 hallmarks of cancer

A 
Sustaining proliferative signalling 
Evading growth suppressors
Resisting cell death 
Activating invasion and metastasis 
Inducing angiogenesis
Enabling replicative immortality
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2
Q

What are the 4 other hallmarks added to the 6 hallmarks

A

Deregulating cellular energetic
Avoiding immune destruction
Genome instability and mutations
Tumour promoting inflammation

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3
Q

What is required to permit the cancer hallmarks

A

Metabolic transformation

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4
Q

What are the 3 nutrients for a cell metabolism

A

Lipids
Carbs
Proteins

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5
Q

What are lipids important in

A

Cell membrane and energy

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6
Q

What is carbs used for

A

Produce DNA, proteins, cell membrane and energy

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7
Q

What are proteins used

A

Brocken into amino acids to produce DNA and energy

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8
Q

In normal cells how is energy obtained in aerobic conditions

A

1) glycolysis: glucose is converted to pyruvate

2) TCA cycle: Pyruvate is metabolised

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9
Q

How many energy i.e ATP is obtained from a normal cell in arerobic condition

A

36 ATP

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10
Q

How does a normal cell obtain energy in anaerobic conditions

A

Glycolysis occurs only

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11
Q

In cancer how is energy metabolised

A

Using glycolysis only even in aerobic condition

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12
Q

At what rate does glycosis in cancer cells run

A

Fast

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13
Q

What is the Warburg effect in cancer

A

when cancer cells switch to glycolysis which occurs in aerobic conditions and produces the breakdown product of lactate as a result

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14
Q

What also the Warburg effect in cancer to take place

A

Activation of oncogenes and/or loss of tumour suppressor genes

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15
Q

What is the role of PTEN

A

To inhibit the PI3K pathway and stop cell survival and proliferation

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16
Q

To make PI3K pathway occur in cancer what can happen to PTEN

A

Mutates to remove its effect

17
Q

If PTEN is removed what protein is activated that removes inhibitory apoptosis protein from BAD so apoptosis is inhibited

A

AKT

18
Q

What other role does active AKT have

A
  • Increases glucose uptake by increasing GLUT-4 on the cell surface
  • Increase the rate of glycolysis by activating the enzyme PFK
19
Q

What are the other way in activating akt

A

Mutation of RAS

20
Q

What is the normal role of P53 in terms of glycolysis and oxidative phosphorylation

A

P53 decreases glycolysis and increases oxidative phosphorylation = opposes effect of the Warburg effect

21
Q

What does P53 help maintain

A

The mitochondria

22
Q

How does P53 maintain oxidative phosphorylation

A

By transcription and activation of SC02 which is a regulator of cytochrome c oxidase complex in the electron transport chain

23
Q

What can happen to P53 in tumours

A

Deficienct i.e knocked out

Mutated

24
Q

What happens if P53 is knocked out

A

TCA is not functional and glycolysis occurs= Warburg effect

25
Q

What happens if P53 is mutated instead

A

It will retain its ability to up regulate enzymes involved in:

1) detox oxidative stress
2) dna/rna synthesis
3) oxidative atp generation
4) increased glucose consumption

26
Q

What does normal P53 do to the uptake of glucose

A

Inhibit the uptake of glucose by inhibiting transcription of glut 1 and glut 4 and glut 3

27
Q

What is c-MHC

A

A gene

28
Q

What does c-myc regulate

A

Lipogenesis
Ribosome genesis
Glycolysis
Glutamineloysis

29
Q

If c-myc is amplified in cancer what does it become

A

An oncogenes

30
Q

What does amplification of c-myc mainly lead to

A

Glutamineolysis

31
Q

What is glutamineolysis

A

Glutamine metabolism

32
Q

What does glutamine metabolism allow in the cancer cell

A

Produce many bio synthetic intermediates to help drive cell proliferation

33
Q

How does K-RAS mutation change metabolism of cancer cells

A
  • Increase uptake of proteins- used to generate new proteins e.g DNA and RNA
  • permanently activate AKT which increases glycolysis
34
Q

In familiar cancer syndrome what happens

A

Enzymes involved in the TCA cycle can become mutation

35
Q

What does mutations of enzymes in the TCA cycle lead to

A

HIF activation

36
Q

What does HIF activate

A

Angiogenesis
Proliferation
Cell survival
Increased glycolysis

CAN (25 decks)

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