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SEM 4:Cellular Pathology > Cellular Growth Regulation > Flashcards

Cellular Growth Regulation Flashcards

1
Q

How does a cell population grow?

A
  • Hyperplasia

- Hypertrophy

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2
Q

Hyperplasia

A

Increase in cell number, tissue growth and most common type of tissue and organ growth.

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3
Q

Hypertrophy

A

Increase in cell size

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4
Q

Example of hypertrophy

A

Heart increase in size due to an increase in cell size not cell number

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5
Q

Describe growth at the cellular level

A

Cell growth is the increase in size (sometimes only) and cell division

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6
Q

Phases of the cell cycle

A

G1, S, G2, and M

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7
Q

What controls the progression of the cell cycle?

A

Restriction points or three key checkpoints

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8
Q

Apoptosis

A

A coordinated program of cell dismantling ending in phagocytosis. Programmed cell death.

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9
Q

When does apoptosis occur?

A

It occurs in response to DNA damage and viral infection

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10
Q

What factors promote growth?

A

Growth factors, cytokines, and interleukins

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11
Q

What are mitogens?

A

Mitogens are proteins that stimulate proliferation and maintain survival.

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12
Q

How are mitogens named?

A

Named after originally identified target e.g. EGF, FGF, interleukins but found to work on other cells other than the ones they have been named after.

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13
Q

Example of a protein that stimulates differentiation and inhibits proliferation

A

TGF beta

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14
Q

Example of a protein that induces apoptosis

A

TNF alpha and other members of the TNF family

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15
Q

What are the three broad classes of factors that promote growth?

A
  • Paracrine
  • Autocrine
  • Endocrine
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16
Q

Paracrine class

A

Produced locally and act on nearby cells - stimulate proliferation of a different cell type that has the appropriate cell surface receptor

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17
Q

Autocrine class

A

Produced by a cell that also expresses the appropriate cell surface receptor

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18
Q

Endocrine class

A

Work like conventional hormones - produced growth factors that work on distant organs and cells (effects).

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19
Q

Describe the cell population growth graph

A
  1. Growth factor added to induce cell number increase
  2. Removing the growth factor will show inhibition in cell growth.
  3. Adding a growth inhibitor will cause the growth of the cells to become stagnant.
  4. A death signal such as TNFa can be added which will decrease the cell number due to apoptosis or necrosis occurring.
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20
Q

When are cell population graphs used?

A

Used in lab when looking at the number of cells over time and the effect of different proteins

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21
Q

Describe the phases of the cell cycle

A 
Mitosis = the production of two daughter cells. One re-enters the cell cycle, starting division and the other becomes a quiescent cell (G0). 
G1 = Cell grows in cell size, DNA - 2N. 
S = Synthesis phase, DNA replication occurs incorporation of thymidine. Cells grow in size as most macromolecules are synthesized continuously throughout interphase. 
G2 = Cells are ploidy, 4N.
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22
Q

What is interphase?

A

Any stage that isn’t mitosis.

23
Q

What are quiescent cells?

A

Cells that can either re-enter the cell cycle when exposed to a growth factor or become terminally differentiated (post-mitotic cells) that undergo apoptosis.

24
Q

What is a fluorescence-activated cell sorter?

A

A machine that uses lasers to measure fluorescence. Cells are in a tube, then fluorescence is measured to show the amount of DNA content or the no. of cells in G1 phase.

25
Q

Describe the graph of cells with low cell division rate

A

60% cells in G1
20% cells in S
20% cells in G2/M

26
Q

Describe the graph of cells with high cell division rate

A

40% cells in G1
40% cells in S
20% cells in G2

27
Q

Summarise DNA replication

A
  1. Semi-conservatively replicates so daughter cells inherit one parental and one new strand.
  2. New DNA is synthesized in the 5’ to 3’ direction from dNTP precursors at the replication fork by a multienzyme complex.
  3. Fidelity is determined by base pairing and presence of a proof-reading enzyme in DNA polymerase
  4. Synthesis of the new DNA strand uses an RNA primer and occurs continuously on the leading strand and discontinuously on the lagging strand forming Okazaki fragments, which are ligated together after removal of the RNA primer.
28
Q

Main stages of Mitosis (Example - answer not written)

A 
Prophase 
Prometaphase 
Metaphase 
Anaphase
Telophase 
Cytokinesis
29
Q

Types of drugs that act on the cell cycle

A

S-phase active

M-phase active

30
Q

Examples of S-phase active drugs

A

5-fluorouracil - an analogue of thymidine that blocks thymidylate synthesis causing it to arrest in S phase as no replication can occur.
Bromodeoxyuridine - an analogue that may be incorporated into DNA and detected by antibodies to identify cells that have passed through the S-phase

31
Q

Examples of M-phase active drugs

A

Colchicine - stabilises free tubulin which prevents microtubule polymerisation and arresting cells in mitosis.
Vinca alkaloids have a similar action to colchicine
Paclitaxel - taxol stabilises microtubules prevent de-polymerisation.

32
Q

What S- and M-phase active drugs are used in treatment of cancer?

A

5-Fluorouracil, Paclitaxel, the vinca alkaloids and tamoxifen

33
Q

What are the cell cycle checkpoints?

A

1) Restriction point to check that DNA is not damaged, cell size and metabolite/nutrient stores
2) Point where DNA is checked to make sure it has completely replicated and DNA is not damaged.
3) Point where chromosomes are checked that they are aligned on spindle.

34
Q

What only happens in G1 phase?

A

Only point of the cell cycle that is responsive to other factors such as growth factors. Main site of control for cell growth

35
Q

What controls the cell cycle checkpoints?

A

Protein kinases and phosphatases that ensure the strict alteration of mitosis and DNA replication

36
Q

What is CDK?

A

10 gene protein Cyclin-dependent kinases that control cell cycle progression. It has a >20 gene cyclin substrate that binds.

37
Q

How are CDK’s activated?

A

By cyclin being bound to it.

38
Q

What does the active cyclin-CDK complex do?

A

It phosphorylates specific substrates.

39
Q

How is the activity of Cyclin-CDK regulated?

A
  • Increase gene expression (cyclical synthesis) and decrease synthesis through destruction by the proteasome
  • Post-translational modification by phosphorylation - depending on the modification site may result in activation, inhibition, or destruction.
  • Dephosphorylation
  • Binding of cyclin-dependent kinase inhibitors which regulate the activity
40
Q

How is the phosphorylation of cyclin changed?

A

The phosphorylation can be changed with phosphatases and protein kinases.

41
Q

Action of RB

A
  1. It is a substrate of G1 and G1/S cyclin-dependent kinase.
  2. In cells in G0/G1; RB binds to transcription factor E2F and inhibits it.
  3. Usually, the cyclin D-CDK-4 and Cyclin E-CDK 2 will phosphorylate RB and it will unbind from E2F.
  4. E2F will be expressed and stimulate the cyclin E and S-phase proteins.
42
Q

What are the two families of cyclin-dependent kinase inhibitors?

A

CDK inhibitory protein/kinase inhibitory protein (CIP and KIP) - also called CDKN1
Inhibitor of Kinase 4 family (INK4 - now called CDKN2)

43
Q

Function of CDKN1

A

Members of this family are stimulated weakly by TGFbeta and strongly by DNA damage (involving TP53)
TP53 releases CDKN1.

44
Q

Function of CDKN2

A

It stimulates the expression of TGFbeta. It specifically inhibits G1 CDKs (e.g. CDK4 the kinase activated by growth factors). This stops the cells from cycling.

45
Q

Summarise how growth factors induce cyclin expression

A

GF binds to GF receptor on the cell as a result, there is an activation of signal transducers. Activate an effect in the nucleus and activate the kinase cascade.

46
Q

Describe the sequential events on the cell cycle

A
  1. G0 receives GF that activates the expression of some genes. This is the initial group of genes called early genes.
  2. Promoters will activate the second wave of delayed genes -> Cyclin D-CDK4/6 complexes.
  3. This will phosphorylate RB so cause gene transcription allowing E2F to work.
  4. As a result, the third wave of E2F responsive genes so most of the proteins required for the S phase are transcribed.
47
Q

When are G1 CDKs activated?

A

In response to environmental signals, late CDKs by preceding kinase activities.

48
Q

What dephosphorylates hyperphosphorylated RB?

A

Protein phosphatase 1.

49
Q

Difference between G1 CDKs and late CDKs

A

G1 CDKs Hypophosphorylate and late hyperphosphorylate

50
Q

What does DNA damage trigger?

A

It triggers cell cycle arrest or apoptosis

51
Q

What is the repair mechanism at the checkpoints? e.g. the two repair outcomes

A
  1. Stop the cycle (cyclin-dependent kinase inhibitors, CHEK2 etc.)
  2. Attempt DNA repair (nucleotide or base excision enzymes, mismatch repair etc.)
  3. Programmed Cell death if repair is impossible (BCL2 family, caspases)
52
Q

What is TP53?

A

A tumour suppressor gene - expressed by all cells.

53
Q

What happens to TP53 when DNA is damaged?

A

If DNA is damaged, TP53 is destroyed so apoptosis occurs. DNA damage is detected by kinases. The kinases add phosphates to TP53 so it is no longer degraded. There is an accumulation of TP53 which activates the expression of CDKN1 inhibitor and stops cell division. TP53 will try to repair DNA so that it is able to enter back into the cell cycle. If repair is not possible, then apoptosis occurs.

SEM 4:Cellular Pathology (13 decks)

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