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BIOL 2321 - Cell Biology > Cell Cycle + Cancer > Flashcards

Cell Cycle + Cancer Flashcards

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1
Q

Describe the cell cycle

A

an ordered sequence of events in which a cell duplicates its contents and divides into two identical cells

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2
Q

What does each cell division produce in a unicellular organism?

A

an entirely new organism

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3
Q

What are cell divisions for in a multicellular organism?

A

countless cell divisions form a zygote

are required for growth

form complex organisms

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4
Q

T or F: as an adult, your cells stop dividing

A

false!! your cells must constantly occur in certain tissues to replace cells that die

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5
Q

What stages does interphase include?

A

G1 (gap 1 for growth)
G0 (not dividing)
S (DNA synthesis)
G2 (gap 2 for growth)

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6
Q

What does the M phase include?

A 
prophase
prometaphase
metaphase
anaphase
telophase
cytokinesis
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7
Q

What would happen if our cells suddenly stopped dividing?

A

we would die in a few days

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8
Q

T or F: the length of the cell cycle varies in different organisms and different cells

A

true

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9
Q

How long is the length of the cell cycle in embryonic cells? Give examples

A

very short

ex. 8 mins in fruit flies
ex. 30 mins in frogs

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10
Q

How long is the cell cycle in mammalian intestinal epithelial cells?

A

12 hours

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11
Q

How long is the cell cycle in human liver cells?

A

~1 year

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12
Q

If cells do not divide, what stage are they permanently in?

A

G0

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13
Q

What does terminally differentiated mean?

A

highly specialized cells (ex. nerve, muscle, red blood cells) are not able to divide

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14
Q

If terminally differentiated cells cannot divide, how are they replaced or repaired when they are damaged or die?

A

they are replenished by stem cell populations as needed

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15
Q

T or F: some cell types can induce non-dividing cells to leave G0 and re-enter G1

A

true

ex. adult liver will divide after injury

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16
Q

Give examples of cell types that are non-dividing but will be induced to leave G0 to re-enter G1

A

adult liver cells will divide after injury

lymphocytes will divide when exposed to specific antigens

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17
Q

T or F: it is common for non-dividing cells to be induced to leave G0 and re-enter G1

A

FALSE! it is rare

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18
Q

List 4 cell types that frequently divide

A

epithelial cells

spermatogonia

stem cells of various tissues (ex. blood)

meristem tissue in the root and shoot tips of plants

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19
Q

Describe multipotent cells

A

stem cells that are highly specialized and can:

self renew and

only produce cell types within one type of tissue or organ

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20
Q

What does totipotent mean?

A

undifferentiated cells which have the potential to become any type of cell

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21
Q

What is progression through the cell cycle primarily controlled by?

A

a group of proteins called Cyclin-Dependent Kinases (CDKs)

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22
Q

What are cyclins?

A

proteins that regulate CDK activity

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23
Q

What is the function of CDK?

A

to phosphorylate various targets in the cell

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24
Q

How are CDKs activated?

A

when cyclin binds tightly to the CDK

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25
Q

Is the concentration of cyclins constant or fluctuating throughout the cell cycle?

A

it fluctuates

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26
Q

What effect does the fluctuation of cyclin levels have on CDK activity?

A

CDK is always present throughout the cell cycle but the activity of CDK will fluctuate with the concentration of cyclin

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27
Q

What are the 3 types of cyclins in the cell cycle and when are they present?

A

G1/S cyclins = active in late G1

S-cyclins = present at S phase

M-cyclins = present at M-phase

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28
Q

What causes the rise and fall of cyclin concentration throughout the cell cycle?

A

the synthesis and degradation of cyclin proteins

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29
Q

What does the rise and fall of cyclin levels cause for CDK activity?

A

rise and fall of CDK activity which promotes cell cycle progression

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30
Q

What causes cyclin levels to fall?

A

cyclin degradation by proteasomes

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31
Q

What causes proteasomes to degrade cyclins?

A

a polyubiquitin chain (molecular tag) is added to a cyclin protein

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32
Q

What is a polyubiquitin chain?

A

a molecular tag made of several ubiquitin molecules added to a substrate like cyclin which targets it to be destroyed in proteasomes, inactivating CDK

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33
Q

How is CDK inactivated?

A

when its bound cyclin is tagged with a polyubiquitin chain, it is targeted to be destroyed by proteasomes and detached from the CDK

unbound CDK = inactive

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34
Q

What adds the polyubiquitin chain to a cyclin?

A

a series of enzymes = E1-E3 ubiquitin ligases

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35
Q

What happens to the degraded cyclin?

A

proteasomes degrade cyclin back into its individual amino acids

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36
Q

Describe the proteasome

A

a compartmentalized protease with sequestered active sites

aka a large protein machine with a central cylinder and stoppers at both ends

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37
Q

What is the proteasome analogous to?

A

a garburator

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38
Q

Where does a protein to be degraded enter the proteasome?

A

through a pore in the stopper into the central cylinder

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39
Q

What forms the central cylinder/chamber of the proteasome?

A

proteases

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40
Q

What direction do the central chamber proteases of a proteasome face?

A

they face the inside of the chamber

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41
Q

Describe how a protein is degraded by the proteasome

A

the stopper proteins of the proteasome bind proteins with polyubiquitin chains and use ATP to unfold them into the chamber

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42
Q

What happens to the ubiquitins attached to a protein to be degraded when it enters the proteasome?

A

they do not enter the chamber and they are recycled

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43
Q

What are the 2 kinases that phosphorylate CDK to activate or inhibit it?

A

activating kinase

inhibitory kinase

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44
Q

T or F: the two kinases phosphorylate CDK at the same site

A

false, at different sites on CDK

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45
Q

Where does the inhibitory kinase add a phosphate on CDK?

A

to the inhibitory P site on CDK

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46
Q

Where does the activating kinase add a phosphate on CDK?

A

to the activating P site on CDK

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47
Q

What is the activity level of a fully phosphorylated CDK (has both inhibitory and activating kinases bound)?

A

partly active

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48
Q

What is required for the CDK to become fully activated?

A

an activating phosphatase must remove the phosphate from the inhibitory P site

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49
Q

What P site will the activating phosphatase dephosphorylate CDK?

A

the inhibitory P site

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50
Q

What is required for the phosphatase to be able to properly function?

A

it must be activated by phosphorylation

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51
Q

How is the phosphatase activated?

A

CDK is a kinase, so it can phosphorylate its own activating phosphatase in order to remove the inhibitory phosphate

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52
Q

What is the purpose of both P sites being phosphorylated if one must be dephosphorylated for full activity?

A

having both P sites phosphorylated means the CDK is partially active

a partially active CDK is required to phosphorylate/activate the phosphatase which can remove the inhibitory phosphate from the CDK and allow the CDK to become fully active

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53
Q

Once the phosphatase is activated, what happens?

A

the phosphatase can activate a LOT of CDK in a short time by removing the inhibitory phosphate = a positive feedback loop

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54
Q

What causes the very steep increase in CDK activity in a cell?

A

the positive feedback loop of the slightly active CDK activating a phosphatase by phosphorylation and then the phosphatase activating the CDK by dephosphorylating the inhibitory P site

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55
Q

What causes the steep decline of CDK activity?

A

proteasome mediate degradation of cyclin

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56
Q

What controls progression through the cell cycle?

A

checkpoints

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57
Q

What occurs at a checkpoint?

A

cell mechanisms pause the progress of the cell cycle if a process has occurred incorrectly or if the conditions are not favourable to progress

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58
Q

What are the 3 main checkpoints?

A

G1 checkpoint: between G1 (or G0) and S phase

G2 checkpoint: between G2 and M phase

M checkpoint: between metaphase and anaphase

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59
Q

What happens if a cell does not pass a checkpoint?

A

the cell cycle is temporarily paused and the cell can use the delay to repair the damage or defect

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60
Q

What happens if the damage or defect of a cell is irreparable?

A

checkpoint mechanisms send out a signal to permanently stop the cell cycle progression or for apoptosis

61
Q

What is another name for the G1 checkpoint?

A

the restriction checkpoint

62
Q

Describe the G1/restriction checkpoint

A

it is the point where the cell is irreversibly committed to cell division

63
Q

At the G1 checkpoint, what are the 3 options?

A
  1. proceed to S phase
  2. pause and repair damage/defect
  3. withdraw from cell cycle and go to G0 if terminally differentiated
64
Q

What 5 things are required at the G1 checkpoint?

A

specific signals (ex. growth factors)

adequate nutrition

sufficient energy reserves

sufficient cell size

undamaged DNA

65
Q

What is the purpose of the G2 checkpoint?

A

to prevent the final entry into the M phase if conditions are not met

66
Q

What 5 things are required at the G2 checkpoint?

A

sufficient cell size

adequate nutrients

sufficient energy stores

**chromosomes have all been replicated

**replicated DNA is not damaged

67
Q

What are the 2 major requirements checked for at the G2 checkpoint?

A

all chromosomes have been replicated

replicated DNA is not damaged

68
Q

Give some examples of different types of damage to DNA

A

single-strand break

mis-matched

damaged base

double-strand break

intra-strand crosslink

inter-strand crosslink

69
Q

T or F: most types of DNA damage can be repaired

A

true

70
Q

Why is it essential that DNA damage is repaired at the G2 checkpoint before the cell enters mitosis or meiosis?

A

because mammalian cells that undergo cell division are more easily transformed into cancerous cells with uncontrollable and unregulated growth and the risk is even higher if DNA is damaged

71
Q

What does DNA damage in mammalian cells lead to?

A

the activation of the p53 protein

72
Q

How is p53 activated?

A

by phosphorylation

73
Q

How often is p53 synthesized? How quickly or slowly is it degraded? What does this result in (in terms of its levels in normal cells)?

A

regularly synthesized + degraded rapidly = low levels in normal cells

74
Q

Is p53 normally high or low in cells?

A

low

75
Q

How is a p53 protein degraded? When does this occur?

A

the protein Mdm2 binds to p53 and promotes ubiquitination so that p53 is degraded by a proteasome

this will happen to p53 when there is no DNA damage

76
Q

What happens when p53 is activated?

A

it is phosphorylated which means Mdm2 cannot bind to it = no ubiquitination = p53 is stable and active and concentrations can rise in the cell

77
Q

Describe p53

A

‘the guardian of the genome’

a transcription factor that is activated and in high concentration when there’s DNA damage

it has many functions in preventing cancer

78
Q

What is the function of p53?

A

to prevent cancer by up-regulating expression of certain genes which prevents the replication of damaged DNA

79
Q

What are 6 specific ways that p53 prevents cancer?

A

when DNA is damaged, p53:

arrests cell division

arrests cell growth

promotes DNA repair

prevents angiogenesis

affects glucose metabolism

can promote apoptosis if needed

80
Q

What is one example of a gene that is regulated by p53?

A

p21

81
Q

Describe what happens when p21 is up-regulated by activated p53

A

p21 will bind to and inhibit the S-cyclin/CDK complex - contributes to arresting the cell cycle when there’s damaged DNA

82
Q

What is the M checkpoint also called?

A

the spindle checkpoint

83
Q

What is the purpose of the M checkpoint?

A

to assess whether all the sister chromatids are correctly attached to spindle microtubules prior to the irreversible splitting during anaphase

84
Q

What can happen if sister chromatids are not correctly attached to spindle microtubules and anaphase occurs?

A

aneuploidy (abnormal chromosome number)

85
Q

T or F: aneuploidy can be repaired

A

false!! this type of DNA damage cannot be repaired because anaphase is not reversible

86
Q

Give an example of aneuploidy and how it occurs

A

Down’s syndrome occurs when there’s an extra chromosome 21

87
Q

What is required at the M checkpoint?

A

all chromosomes are properly attached to the spindle microtubules

88
Q

Where does the cell progress if it passes the M checkpoint?

A

completes mitosis from anaphase onward

89
Q

T or F: most cells arrest the cell cycle once they have differentiated

A

true

90
Q

What can happen to a cell if the cell cycle doesn’t arrest when it should?

A

that cell can become cancerous

91
Q

Why is it called cancer?

A

because cancer means ‘crab’ and the cells that invade surrounding tissues have projections that look like pincers

92
Q

What causes cancer?

A

uncontrolled cell division arising from a single cell that contains mutations in specific genes = the original cell and all daughter cells ignore normal cell division checkpoints

93
Q

What are the 2 basic properties of cancer?

A

uncontrolled growth

ability to invade and colonize areas normally reserved for other cells

94
Q

T or F: cancer is genetic and therefore always heritable

A

false. cancer is genetic but it is not usually inherited

95
Q

How does most cancer arise?

A

usually not in germ-line cells (not heritable)

usually in somatic cells during an individual’s lifetime from errors in DNA replication

96
Q

What 2 things affect mutation rates? give examples

A

cellular environment
mutagens

ex. UV radiation, chemical exposure, radiation, heat, cigarette smoke, pollution, age, genetics

97
Q

Approximately how many Canadians will develop cancer in their lifetime? Why is this number actually not as large as it could be?

A

2 in 5

when you consider that we have trillions of cells and there’s billions of cell divisions every dat with a guaranteed rate of mutation and mutagens increase that basal rate, 40% is actually not that big

98
Q

Why does the risk of cancer increase with age?

A

because you need a substantial number of mutations in a single gene to occur in order to develop a cancerous tumour and rate of mutations increases with more cell divisions

the longer you live, the more cell divisions occur = more mutations

99
Q

What tissues do the most common cancers arise in? Why? Give examples

A

in epithelial tissues because these cells undergo a relatively high level of cell division

ex. breast, colon, prostate, lung

100
Q

What are some examples of behaviours of cancer cells as a result of their mutations?

A

unresponsiveness to external signals

loss of attachment to ECM and substrata

no contact inhibition

no regulation of cell division

avoidance of apoptosis

lack of differentiation

ability to enter and survive in foreign tissues

101
Q

Why is the loss of attachment of cancer cells to the ECM bad?

A

this allows them to spread and invade other areas

102
Q

What does no contact inhibition mean in regards to cancer cells?

A

they do not stop growing when they touch other cells = this results in tumours

103
Q

Why is it bad that cancer cells do not differentiate?

A

because differentiation would normally stop cell division = another way they maintain uncontrolled division

104
Q

What are 3 ways in which cancer cells are able to enter and survive in foreign tissues?

A

they can survive with low oxygen away from blood vessels

they can bypass cell-cell junctions and create intercellular pathways

they can secrete proteases to degrade the ECM

105
Q

How many layers do normal cells grow in a petri dish? What about cancer cells? Why?

A

normal: 1 layer thick because they stop growing when they touch each other (contact inhibition)
cancer: multiple layers because they do not have contact inhibition and can pile on top of each other

106
Q

T or F: mutations that result in cancer are always in genes that somehow affect cell division

A

true

107
Q

What are the 2 kinds of genes that relate to cancer?

A

tumour suppressor genes

protooncogenes

108
Q

What is the normal function of tumour suppressor genes?

A

to restrict the cell cycle

109
Q

What is an example of a protein coded for by a tumour suppressor gene?

A

p53

110
Q

What happens when there’s mutations in a tumour suppressor gene?

A

the genes are turned off and the cell cycle is not restricted = cells can divide without needing to pass checkpoints which can lead to replicating damaged DNA

111
Q

What kind of genes are considered tumour suppressor genes?

A

ones that promote differentiation

112
Q

What kind of mutation occurs when a tumour suppressor gene is mutated?

A

a loss of function mutation

113
Q

How many alleles need to be mutated in a tumour suppressor gene to result in a loss of function?

A

both

114
Q

What is the normal function of proto-oncogenes?

A

to promote cell division

115
Q

What is an example of a protein that is coded for by proto-oncogenes?

A

CDKs

116
Q

What happens to proto-oncogenes when they are mutated?

A

they are turned on permanently and they are not regulated properly = constant cell division

117
Q

What kind of a mutation results when a proto-oncogene is mutated?

A

gain of function

118
Q

What are proto-oncogenes called after they are mutated?

A

oncogenes

119
Q

How many alleles must be mutated to result in a mutated proto-oncogene?

A

only one

120
Q

What does mutations in both proto-oncogenes and tumour suppressor genes cause?

A

tumour growth

121
Q

What are 4 examples of mutations to a proto-oncogene that can turn it into an oncogene?

A

deletion or point mutation in coding sequence

regulatory mutation

gene amplification

chromosome rearrangement

122
Q

What are 3 examples of genes that can be mutated to cause cancer?

A

cell signalling pathway genes (ECM signals, survival signals, growth + differentiation signals) - ex. RTK

cell cycle regulation genes (checkpoint genes)

apoptotic genes

123
Q

What is the most commonly mutated gene in human cancers?

A

p53

124
Q

in what ways are cancer cell genomes unstable?

A

they have big genomic changes and often show abnormal chromosomes with large deletions, translocations, inversion, and excessive heterochromatin

125
Q

In a karyotype, how would you know if you’re looking at a cancer cell genome?

A

the chromosomes will be multiple colours due to a lot of rearrangement

126
Q

What are two words for a cluster of abnormal cells growing out of control?

A

tumour or neoplasm

127
Q

What are the 2 types of tumours?

A

malignant

benign

128
Q

What is the major similarity and difference between malignant and benign tumours?

A

Similarity: they are both clusters of abnormal cells growing out of control

Benign tumours are not yet invasive

malignant tumours are cancerous because they are invasive

129
Q

Describe benign tumours

A

slow-growing, non-invasive cluster of abnormal cells growing without regulation

130
Q

What can limit the growth of benign tumours?

A

being covered by connective tissue sheaths

131
Q

Are benign tumours generally easy or difficult to remove? why?

A

they can be covered and therefore isolated in a connective tissue sheath = clean edges and easy to remove

132
Q

T or F: the removal of a singular benign tumour usually results in a complete cure

A

true

133
Q

How can benign tumours be harmful?

A

they can compress adjacent tissues and block important structures with important functions (ex. trachea or a lumen)

if the tumour is of endocrine tissue it could result in uncontrolled hormone secretion and cause disease

they have a high likelihood of becoming cancerous

134
Q

Explain why malignant tumours are always harmful

A

they are invasive so they can disrupt the tissue and spread (usually by losing attachment to ECM or basement membrane) and metastasize by entering blood or lymph and move around the body

135
Q

Describe the process of cancer

A

a single mutation in a single cell which promotes growth or division will produce a lot of daughter cells

daughter cells accumulate their own mutations

each mutation increases ability of the cancer cell to grow, divide, evade apoptosis, and invade other tissues

136
Q

How many mutations do cancers usually carry? Are they dependent or independent mutations? Are they common mutations?

A

usually many independent, rare mutations

137
Q

Describe angiogenesis

A

the development of new blood vessels

138
Q

How do large tumours metastasize?

A

they form their own vasculature (angiogenesis) to help them receive oxygen and perform lots of cellular respiration to produce lots of ATP = lots of growth

139
Q

Where does the development of blood vessels occur in an embryo?

A

in every part of an embryo

140
Q

What drives the development of blood vessels in an embryo?

A

a growth factor called VEGF

141
Q

Describe VEGF

A

A growth factor / ligand that binds to RTKs and activates signalling pathways

it drives the development of blood vessels

142
Q

How do growing tumours perform angiogenesis?

A

they express VEGF, the growth factor that signals for the development of blood vessels

143
Q

Describe the process of metastasizing

A

a growing tumour expresses VGEF which induces blood vessels to form and invade the tumour mass = allowing the tumour to conduct cellular respiration and produce ATP to grow –> tumour can metastasize and move through the blood to other parts of the body

144
Q

What are metastases?

A

secondary tumours

145
Q

T or F: a primary tumour is usually traceable from metastasis

A

true

146
Q

Are metastases usually removable by surgery?

A

No

147
Q

Is it generally metastases or the primary tumour that results in the death of a cancer patient?

A

metastases

148
Q

How can tumours effect organ function?

A

Once a primary or secondary tumour reaches a significant mass, the organ can no longer function properly

BIOL 2321 - Cell Biology (26 decks)

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