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Chronic Disease > Selenium And Cancer > Flashcards

Selenium And Cancer Flashcards

1
Q

In genetics lecture. What defined tumorigenesis

A

Mutations and damage leading to proliferation signalling, angiogenesis, resisting cell death, metastasis

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2
Q

What is selenium

A

A micronutrient needed for selenoprotein synthesis

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3
Q

Name some anti carcinogenic properties of seleniproteuns

A

Antioxidants (ox stress causes cancer)

Immune surveillance

Er stress response

Tumour suppressive/anti proliferation and survival

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4
Q

What are the major antioxidant proteins

A

Gpx

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5
Q

Where is deficiencies seen due to poor soil content

A

Europe , China and nz

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6
Q

Explain the small benefit risk window

A

Deficiency causes diseases like keshans

Suboptimal- increased cancer, cvd and t2d risk

Diabetes seen in supra optimal SELECT study

And selenosis/toxicity in high levels

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7
Q

What do all selenoproteins need to share forking the hierarchy

A

The selenium is contained in form of selenocysteine (sec amino acid) incorporated during translation

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8
Q

Which stop codon in selenoproteins read to incorporate sec instead

A

Uga

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9
Q

What does selenoproteins mrna have in 3’ utr

A

Secis

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10
Q

Explain briefly the steps of translation

A

Ribosome reads uga and recruits trna sec
It binds to secis
Sec is then incorporated into selenoproteins

Secis needs bound factors like sbp2 and ef which then allows the sec incorporation as it allows recoding uga into a non Stop codon

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11
Q

What happens to proteins low in hierarchy

A

If not enough sec, uga is a stop codon and truncated protein is degraded

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12
Q

What are some proteins high in hierarchy

A

Sep15 - er stress
Gpx4 - antiox

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13
Q

What are some low

A

Gpx1

SelS (er)

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14
Q

Why might selenoproteins be linked to cvd

A

Oxidative stress causes damage to vascular endothelial cells exacerbating issues like atherosclerosis

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15
Q

What does selS knockout do when er stress builds

A

Activation of inflammatory pathways like nfkb and apoptosis dysregulation

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16
Q

What did the npc us study find

A

In those with baseline low se levels, pca and crc risk reduced when given supplements

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17
Q

Why did the select study counteract this

A

Found no effect on pca risk but increased t2d risk instead

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18
Q

Why did this study differ

A

Ppts we’re already high in selenium baseline

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19
Q

What did these studies spark

A

Interest in genetic factors affecting requirements for se

Need to test previous se levels because of the small window

20
Q

What study type was used to study sep15 snps in prostate cancer

A

Candidate

21
Q

What is sep15 relevance in prostate cancer

A

Helps protein folding and involved in er response
Highly expressed in prostate

22
Q

Which 2 variants found

A

Intron variant (gene exp affected in selenium presence)

3’ utr affecting sec incorporation

23
Q

What did this study conclude from selenium intake

A

The supplement only improved for those with the ga/gg genotype

As increased survival rates

No effect for A/A

Hence need genotyping before supplementation

24
Q

Which plasma selenoprotein is responsible for delivering se for other protein Stnrhesis

A

Sepp/ selenoprotein P

25
Q

Which 2 isoforms exist

A

60kda (has 10sec )

50kda (1 sec)

26
Q

How many snps were found in this sepp

A

2, 1 in coding region ala234thr, 1 in 3’ utr

27
Q

What did these affect

A

Sepp isoform patterns, levels of sepp in general, se availability for other proteins

28
Q

What proteins affected by this reduced sepp1

A

Gpxs and tr1

29
Q

Which other snp in Sweden found to interact with the ala234 sepp1 snp to greater increase pca risk and what does the snp do

A

Sod2 (gain of function meaning more h202 made from superoxides)

30
Q

Why is sepp1 needed to get rid of excess h202

A

Gpx needs sepp1 and gpx allows conversion of h202 to water

31
Q

Why would excess h202 be a problem

A

Causes pca cell proliferation and migration

32
Q

Why is this relevant to se supplements

A

Because Sweden is low in se to begin with… maybe increasing it would counteract sepp1 bioavailability

33
Q

What does the gpx4 snp do

A

Affects incorporation of sec
Affects the 3’ utr sequence
Affects its position in the hierarchy during low selenium

34
Q

How does the TT affect sec incorporation

A

Reduced affinity of synthesis machinery for secis

35
Q

During low selenium, which other proteins became higher in the hierarchy than gpx4

A

Gpx1 and 3

36
Q

Where was the study into many snps and crc risk done

A

Czech with low selenium levels

37
Q

Before 2 loci interactions were studied, which 3 snps impacted risk

A

SelS, sepp1, gpx4

38
Q

What 2 loci interactions were found ALONGSIDE THE LOW SE LEVELS

A

Sepp1 (affecting bioavailability)

And either gpx4 (antiox) or sep15 (er stress)

39
Q

Why would this favour cancer switch

A

Build of ox and er stress

40
Q

What did gwas help find se metabolism snps linking to which disease

A

Ibd / crohns and gpx snps

41
Q

What was the Nutri genomic approach important for

A

Study the pathways nutrient se levels affects gene exp of

42
Q

Give examples of the types of genes and proteins affected by nutrient se suboptimal levels

A

Cancer pathways, immune proteins, genes in cell movement/apoptosis, proliferation/growth, inflammatory pathways

43
Q

What sorts of events caused from suboptimal se

A

Inflammatory dysregulation
Reduce dimmune system capacity
Cytokseletal remodelling/loss of barrier

44
Q

What sorts of genes were affected which reduce ability of immune system to deal with pathogens causing inflammation

A

Nfkb, il1b,il 8

Complement c3

45
Q

What sorts of proteins were affected by se status

A

Actin, tubulin, cyotkeratins (all cytoskeleton proteins)

Chronic Disease (16 decks)

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