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Anatomy and Physiology I > Exam 3: Cell Cycle > Flashcards

Exam 3: Cell Cycle Flashcards

1
Q

Where do most cells spend 80% of their cycle?

A

interphase

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2
Q

cells like skeletal muscle and neurons can enter what stage?

A

quiescence G0, stay in interphase

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3
Q

3 stages of interphase

A

G1, S, G2

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4
Q

G1

A

newly formed cell enters stage and begins to express genes to carry out function. Most metabolic function, house keeping stuff of the cell, if differentiated into skeletal muscle cells or cardiac muscle cells neurons will not progress, stay in G1, permanently in G0

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5
Q

S

A

the synthesis stage in which DNA replication occurs

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6
Q

G2

A

cell prepares for division
production of proteins (tubulin, kinetochores) needed for division increase
organizational phase

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7
Q

what is the progression through interphase controlled by?

A

cyclin-dependent kinases and cyclins

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8
Q

cyclin-dependent kinases (cdk)

A

apoenzymes relatively constant throughout the cell cycle

- take phosphate group off one molecule and put it on another

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9
Q

cyclin

A

coenzymes that fluctuate during the cell cycle activating cdks
- cyclin and cdk come together to get a holoenzyme, target protein to do phosphorylation

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10
Q

the movement of cells through interphase can be affected by what?

A

growth factors and tumor suppressors

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11
Q

growth factors

A

increase rate through interphase

- wound healing

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12
Q

tumor suppressors

A

decrease or stop progression, can cause apoptosis

  • the brakes to a car going down the road
  • blebs coming off of it
  • cancer apoptosis
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13
Q

G1 to S initially

A

E2F/DP dimer inactivated by RB
cdk 4 and cdk 6 unbound
cyclin D levels low

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14
Q

G1 to S stimulation

A

cyclin D level increases

binds to cdk 4 and 6

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15
Q

G1 to S progression

A
  • cyclin D complex phosphorylates RB
  • E2F/DP dimer released and active
  • E2F/DP transcription factor for cyclin E
  • cyclin E forms complex with cdk 2
  • cyclin E complex initiates S phase
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16
Q

How does E2F/DP get shut down

A

RB starts out as a brake, bound to E2F when nothing is going forward the cell is simply in G1

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17
Q

What helps to increase cyclin D?

A

estrogen receptors

if cell damage, prostaglandins form COX2 pathway which can inc it

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18
Q

S to G2 initially

A

cyclin E complex moves S phase forward

- E2F levels rise and binding is done to inc cyclin A

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19
Q

Which cyclin outcompetes which?

A

A outcompetes cyclin E

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20
Q

S to G2 progression

A
  • E2F/DP level rises
  • E2F/DP transcription factor for cyclin A
  • cyclin A outcompetes cyclin E for cdk 2
  • cyclin A forms complex with cdk2
  • cyclin A complex phosphorylates E2F
  • E2F/DP inactive
  • S phase complete
  • cyclin A complex initiates G2 phase
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21
Q

what initiates the G2 phase

A

the cyclin A complex once cyclin A outcompetes cyclin E

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22
Q

G2 to M initially

A

cyclin A complex phosphorylates cdc 25

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23
Q

phosphatase

A

it will put on or take off phosphates but does not transfer phosphate groups to another molecule

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24
Q

Cyclin B

A

constant, increase
its kinase is shut down
dephosphorylate cdk 1

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25
Q

G2 to M progression

A
  • cdc25 activated
  • cdc25 dephosphorylates cdk1
  • cdk1 forms complex with cyclin B
  • cyclin B complex initiates M phase
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26
Q

what is the MPF (M-phase promoting factor)

A

cdk1 cyclin b complex

27
Q

Primary System - pRB

A
  • inhibits transcription factor E2F
  • acts at onset of cell cycle
  • names for research in retinal blastoma
    found in all cells
28
Q

Secondary System - p53

A
  • transcription factor
  • inhibited by mdm2
  • low p53 promotes p21 expression
  • p21 interferes with cdk2 binding (extends S)
  • high p53 promotes BAX expression
  • BAX promotes apoptosis
29
Q

when does the secondary system kick in?

A

only comes in when damage to cell and need extra time

  • emergency braking system
  • transcription factor you keep quiet until needed (mdm2 is its inhibitor)
30
Q

when damage to cell, inactivation of mgm2 and what is released

A

p53
- small amounts of p53 promote p21 which interferes with cdk2 binding - cannot bind cyclin A - cannot finish s phase - gives more time to correct mistakes

31
Q

if too much damage (p53)

A

p53 getting too high, get BAX gene which attacks the mitochondria and kills the cell
- since not repairable it kills itself

32
Q

what happens in cells existing in G0

A

p16 an inhibitor that binds to cdk 4 preventing activation of E2F

33
Q

Normal growth factors

A
  • PDGF and EGF increase levels of E2F
  • proto-oncogenes regulated
  • estrogen increases production of cyclin D
34
Q

PDGF

A

platelet derived growth factor for healing

35
Q

proto-oncogenes

A

only expressed in diff times in development - early

36
Q

Abnormal growth factors

A
  • oncogenes unregulated
  • upregulation of estrogen receptors
  • disruption of tumor suppressors
37
Q

disruption of tumor suppressors

A

mutation
infection
chronic inflammation

38
Q

oncogenes

A

upregulated proto-oncogenes , turned on when they shouldn’t

- rapid uncontrolled cell growth

39
Q

upregulation of estrogen receptors

A

check to see if cancer has increased estrogen receptors

- they can check with estrogen blockers

40
Q

benign tumor

A

can still produce adhesion molecules and stay together

41
Q

hyper-mitotic

A

fast growing but benign

42
Q

Polyp

A

raised form can be either benign or cancerous

43
Q

Precancerous

A

some morphological changes from cells of origin, but still adheres together

44
Q

Cancer

A

morphological changes obvious, not adhering

45
Q

Stage 0

A

-caught at earliest, still in tissue where it formed

0 small not invasive tumor

46
Q

stage 1

A

small and invasive to immediate surrounding tissue

47
Q

difference between stage 1 and stage 2?

A

stage 2 is not worse, it is done by size, so stage 2 is larger in mm than stage 1

48
Q

stage 2`

A

large and invasive to immediate surrounding tissue

49
Q

stage 3

A

invasive to local lymph nodes
- if find in lymph node you know the cancer cells changed enough to no longer recognize cells they came from, metastasizing

50
Q

stage 4

A
  • invasive to distant tissue

- metastasized beyond lymph nodes

51
Q

Application: Pharmacology Targets for Cancer

A
  • cyclin D dysregulation can lead to progression of types of cancer
  • goes through too fast, can make mistakes
52
Q

Application: Pharm targets for cancer

How do the following targets lead to a dec in cyclin D?

A

kinase inhibitors stop the initial kinase from binding cyclin D
- block estrogen
radiation, immunotherapy go after cyclin D
- competitive binding inhibitors prevent binding of cdk4 and cdk 6 which blocks cyclin D from forming its complex

53
Q

Application: pharm in cancer

how would this affect target cell’s cycle of development?

A

cdk inhibitors to inhibit cdk 2 - cannot enter the S phase

54
Q

Application Ulcerative Colitis

Explain why ulcerative colitis is associated with an inc risk f colon cancer?

A

has chronic inflammation inc the risk, does not cause cancer
- release of signaling inc the cell cycle, setting up environment where if mistakes happen you could be at risk for cancer

55
Q

Why would someone who has irrital bowel syndrome can have similar discomfort but not an increased cancer risk?

A

the inflammation would draw growth factors from mitosis

- lower risk of cancer with anti inflammatory drugs

56
Q

Application: Cancer

A

mutation in BRCA1 gene affects binding of RB to E2F/DP

57
Q

How does BRCA1 normally enhance binding?

A

slowing the phosphorylation of the complex

- slows release of transcription factor slowing down cell cycle, enhancing primary braking system RB

58
Q

BRCA 1 mutation compared to defective p53

A

similar: both phases S phase effected - inc risk of errors to go through for both
- differences: p53 slows down S phase (if defect you would not be able to slow it down)
- in BRCA defect S phase would speed up, less time to avoid mutations
- defect in p53 lose ability to do apoptosis

59
Q

Application: Triple Negative Breast Cancer

A

triple negative cells have no marker, no estrogen or hormone receptors, no epidermal growth factor receptors

60
Q

challenges for triple negative breast cancers?

A

nothing to inhibit - no receptors to block.

- you cut out what you can find, use chemo and radiation

61
Q

HER2

A

forms heterodimer as normal receptor

  • when binds epidermal growth factor triggers cell to put out more cyclin D
  • constantly going through mitosis without signal
62
Q

Application: Cancer and Viruses

2 ways HPV increases risk of cancer

A
  • HPV gene 6 inactivates p53

- HPV gene E7 inactivates pRB

63
Q

Application: explain how inactivating p3 and pRB would effect the cell cycle and inc cancer risk?

A

inactivating p53: cannot do apoptosis, take out potentially cancerous cells
inactivating pRB: cannot end S phase - replicating too fast causing mistakes

64
Q

What does HPV take out?

A

both braking systems primary (pRB) and secondary (p53)

speeds up cell cycle can not slow down if mistakes

Anatomy and Physiology I (17 decks)

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