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Chronic Disease > Selenium, Cancer and Nutritional genomics from SNPs to molecular pathways > Flashcards

Selenium, Cancer and Nutritional genomics from SNPs to molecular pathways Flashcards

1
Q

What is cancer?

A

Multi-steps process; accumulation of genetic mutations leads to acquisition of tumour phenotype

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2
Q

What kinds of mutations can cause cancer?

A

Increase in cell survival or loss of cell death

Inhibition of repair mechanism, tumour suppressors or immune response

Decrease of genetic stability

Increase in angiogenesis

Increase in mobility

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3
Q

What is angiogenesis?

A

Formation of new blood cells

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4
Q

What are the main cancer prevention mechanisms?

A

Antioxidant mechanism

Tumour suppressor genes

Repair mechanism

Immunosurveillance

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5
Q

What is selenium?

A

AN anticarcinogenic trace element.

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6
Q

What kind of food is selenium rich?

A

Seafood

Nuts

Red meat

Eggs

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7
Q

What is the recommended uptake of Selenium for men per day in the UK?

A

75 micrograms

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8
Q

What is the recommended dose per day for women of selenium?

A

60 micrograms

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9
Q

Why is it important to maintain the optimal Selenium intake?

A

Required to support synthesis of selenoproteins

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10
Q

How many selenoproteins are there in humans?

A

25

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11
Q

What are the key roles of selenoproteins in cancer prevention mechanisms?

A

Anti-oxidant defences and redox signalling

Tumour suppression and control of survival

ER stress response

Immune system activation

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12
Q

How do selenoproteins support anti-oxidant defences and redox signalling?

A

Protect against oxidative damage in cytoplasm and mitochondria.

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13
Q

How do selenoproteins support ER stress response?

A

Proteins folding/removal of misfolded proteins.

Involved in ca2+ signalling.

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14
Q

What is the direct role of selenoproteins in tumour-suppression?

A

Act as tumour supressors

Activate other tumour suppressors

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15
Q

Which selenoproteins act as tumour supressors?

A

SELENOP

GPx3

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16
Q

Which tumour suppressors do selenoproteins activate?

A

p53

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17
Q

Which selenoproteins limit survival and proliferation of tumour cells?

A

GPx1

GPx4

SELENOP

SELENOF

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18
Q

What is the direct role of selenoproteins in immunosurveillance?

A

Activate the removal of the tumour cell by the immune system.

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19
Q

Which selenoproteins have a role in immunosurveillance?

A

SELENOP

TXNRD

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20
Q

Which selenoproteins act as antioxidant enzymes?

A

GPx

TNXRD

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21
Q

What is the geographical issue with selenoprotein?

A

Some areas have Se poor soil therefore that population will have lower Se intake.

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22
Q

What is the link between selenium intake and disease risk.

A

A very narrow risk-benefit window.

Too little, increases disease risk due to suboptimal intake.

Too much, increases disease risk, toxicity.

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23
Q

What happens when Se suboptimal?

A

Increased risk of cancer, type 2 diabetes, cardiovascular disease, dementia and risk of infection.

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24
Q

Why is the dose-response being a U shape difficult for treatment?

A

The optimal will be different for individuals.

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25
Q

What is the role of selenoproteins in the body?

A

Mediate Se biological actions using Se biological actors

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26
Q

How do selenoproteins contain Se?

A

In the form of the amino acid selenocysteine (Sec).

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27
Q

When is Sec incorporated into selenoproteins?

A

Sec incorporated in nascent
selenoprotein protein sequence during translation

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28
Q

What are the 2 main characteristics of selenoprotein charecteristics?

A

UGA codon, coding for Sec

SECIS stem loop RNA structure in 3’UTR

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29
Q

What does SECIS stand for?

A

SElenoCysteine Insertion Sequence

30
Q

How does selenoprotein synthesis happen? (4 steps)

A
  1. Recruit tRNA(sec)
  2. Bind to SECIS
  3. Sec incorporated into selenoprotein
  4. Protein synthesis continues till STOP codon.
31
Q

What does it mean that the selenoproteins have a hierarchy when Se levels are suboptimal?

A

Reduced Se means a reduced Sec bioavailability, sharing of Sec follows a hierarchy.

32
Q

How are the selenoproteins low in the hierarchy stopped from being produced?

A

UGA codon signals ends on translation

Truncated proteins degraded

33
Q

Which selenoproteins are high in the heirarchy?

A

GPx4

SEP15

34
Q

Which selenoproteins are low on the hierarchy?

A

GPx1

SelS

35
Q

What is the problem with Se supplementation trails?

A

Have conflicting results.

36
Q

How do we advise people on Se supplementation?

A

Personal advice, due to the optimal varying in individuals.

37
Q

Which selenoprotein functional SNPs were found to cause colorectal cancer in the czech cohort ?

A

SEPP1

SELS

GPX4

38
Q

Which selenoprotein functional SNPs were found to cause to find breast cancer in the danish cohort?

A

SEPP1

GPX1

39
Q

Which selenoprotein functional SNPs were found to cause to find prostate cancer in the german cohort?

A

SEPP1

GPX1

40
Q

Which selenoprotein genes were found to cause to find prostate cancer in the German cohort through pathway analysis?

A

SELK

TXNRD1

TXNRD2

41
Q

What does epidemiological data say about the role of SE in the protection against Prostate Cancer?

A

NPC trial decrease of prostate cancer when a low baseline Se levels.

SELECT trials prove supplementation has no effect on prostate cancer but increases the risk of type 2 diabetes in high Se status.

42
Q

What is SEP15?

A

15kDa selenoprotein highly expressed in prostate tissue.

43
Q

What gene codes for SEP15?

A

SELEOF gene

44
Q

What is SEP15’s role?

A

Protein folding control in the ER and ER stress response.

45
Q

Which SNP affects the activity of SEP15?

A

(A/G)

46
Q

How does the SEP15 SNP affect who we can and cant supplement?

A

AA types have a higher mortality than benefit than GG/GA in high Se plasma status

Some benefit for GG/GA in high Se for prostate cancer risk

47
Q

What is SePP?

A

60% of all plasma Se

Best biomarker of active Se

48
Q

Where is Sepp synthesized?

A

Liver from dietary Se

49
Q

What is the role of SePP?

A

Secreted in the plasma

Transports hepatic Se to other organs for synthesis of other selenoproteins.

50
Q

What are the 2 plasma isoforms of SePP?

A

60kDa (10sec)

50kDa

51
Q

Where are the 2 common SNPs in the SEPP1 gene?

A

In coding region

In the 3’UTR

52
Q

What happened when SePP1 SNP individuals were supplemented with Se?

A

The effect of the SNPs disappears in Se supplemented volunteers.

53
Q

What is Glutathione Peroxidase 4 (GPx4)?

A

Key enzyme in redox control and antioxidant defence in cytoplasm and mitochondria.

54
Q

The rs713041 (C/T) in the GPX4 gene affects?

A

The sequence of GPX4 mRNA in 3’UTR, this is close to SECIS

The incorporation of Sec into GPX4 during translation

Position of GPX4 in the hierarchy

55
Q

What do those carrying the C variant of the GPX4 gene have that those who have the T variant don’t?

A

Selenoprotein synthesis machine has a stronger affinity for SECIS in C.

C had a greater ability to promote Sec incorporation in GPX4

56
Q

What does the presence of the T variant do for GPX4 in the selenoprotein hierarchy?

A

CC carriers are synthesised more than those of TT.

57
Q

What is GPX1?

A

Oxidative stress response

58
Q

Where are the functional SNPs for SEPP1?

A

Promoter

3’UTR

Coding SNP

59
Q

Where are the functional SNPs for GPX4?

A

3’UTR

60
Q

Where are the functional SNPs for SEP15?

A

3’UTR

Intron

61
Q

Where are the functional SNPs for GPX1?

A

Coding SNP

62
Q

What SNPs were found to have an effect on the risk of prostate cancer when genetic association was studied using the pathway analysis?

A

2 functional SNPs in SEPP1 and GPX1.

63
Q

What tagSNPs were found to have an effect on the risk of prostate cancer when genetic association was studied using the pathway analysis?

A

SELK

TXNRD2

TXNRD1

64
Q

What was the strategy for genetic association was studied using the pathway analysis in prostate cancer and selenoproteins?

A

384 tagSNP to capture genotype of all SNPs in 72 genes in whole Se metabolic pathway

65
Q

Define GWAS?

A

Powerful approach to identify novel target/novel pathway influencing common diseased, but only explain a small fraction of the inherited risk.

66
Q

What is the downfall of GWAs?

A

Some of the missing inherited risk can be attributed to gene X nutrient interactions.

67
Q

What are the steps to studying the impact of nutrient on gene expression.

A
  1. Nutritional phenotyping
  2. Bioinformatics to compare experimental knowledge to database
68
Q

What is NF-kB?

A

A transcription factor with a key role in inflammatory and immune response, cell survival and apoptosis.

69
Q

Why is NF-KB important?

A

Impaired regulation leads to cancer development and progression.

70
Q

How does NF-KB inhibition affect Selenoproteins?

A

Leads to the inability of individuals of suboptimal Se to respond to stress, pathogens and homeostasis.

71
Q
A

Chronic Disease (15 decks)

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