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Cell Biology > Exam 4 (Baines + Bowles) > Flashcards

Exam 4 (Baines + Bowles) Flashcards

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1
Q

What is the Warburg Effect?

A

tumor cell has HUGE increase in glucose uptake to meet metabolic demand

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2
Q

Tumor cells need (less/more) glucose to get same ATP as normal cells because they undergo ____.

A

More
anaerobic glycolysis

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3
Q

Warburg Proposal for Cancer

A

cancer caused by damage to ETC
cancer cells use anaerobic glycolysis to compensate for lack of oxygen (sually produced by ETC)

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4
Q

How does PET scan detect cancer?

A

fluorine added to glucose (FDG)
taken up in part of body where glucose taken up
prominent fluorine = potentially cancerous

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5
Q

Why use PET + CT scan?

A

better anatomical location for exact location of cancer

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6
Q

Tumor cells produce ___ so normal cells near them cannot survive.

A

lactate = acidic environment

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7
Q

List 2 environmental advantages of tumor cells

A
  1. lack of oxygen
  2. acidosis
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8
Q

Cancer cells need _____, so they activate ______ to make cell membranes for new cells / cell proliferation.

A

lipids
lipid synthesis

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9
Q

What are the two major metabolites relied on for a proliferating cell?

A

Glucose
Glutamine

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10
Q

What pathways is associated with glutamine (used by proliferating cells)?

A

Ras/Raf/MEK/ERK pathway

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11
Q

Ras/Raf/MEK/ERK pathway mechanism

A

glutamine activates KGA
KGA converts glutamine –> glutamate
glutamate converts to TCA + ATP
= cell growth / proliferation

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12
Q

Proliferating cells have a high demand for ____ due to their need for lipid synthesis & protein synthesis

A

NADPH

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13
Q

How is skeletal muscle associated with metabolism in cancer?

A

glutamine + amino acids come from skeletal muscle mass of cancer patients

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14
Q

How is adipose tissue associated with metabolism in cancer?

A

uses lipids from adipose to make cell membrane for proliferating tumor cells

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15
Q

How is the liver associated with metabolism in cancer?

A

Cori Cycle- gluconeogenesis –> new glucose from lactate

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16
Q

A mutated nuclei put in a normal cell (converts/doesn’t not convert) it into a tumor cell

A

does NOT convert

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17
Q

A normal nuclei put in a tumor cell (converts/doesn’t convert) it back into a normal cell

A

doesn’t convert

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18
Q

What is the metabolic cause for cancer?

A

mitochondria

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19
Q

What is different about the mitochondria in the cancer cell?

A

NO cristae so ETC cannot occur

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20
Q

What are two dietary cancer therapies focused on metabolism?

A
  1. Ketogenic diet (“starve” cancer cells of glucose)
  2. Restrict overall food intake
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21
Q

What are 3 pathways that are metabolic targets for cancer treatment?

A
  1. Inhibit PFK-B
  2. Inhibit Acetyl-CoA carboxylase
  3. Inhibit Glutamine Metabolism
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22
Q

Mechanism for inhibiting PFK-B for cancer cell treatment

A

cancer cells express PFK-B (not in normal cells) that regulates glycolysis
drug inhibits PFK-B –> starve tumor cells

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23
Q

Mechanism for inhibiting Acetyl-CoA carboxylase

A

drug inhibits ACC = reduced cancer cells
disadvantage- also blocks normal cell fat synthesis

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24
Q

Mechanism for inhibiting glutamine metabolism

A

drug inhibits glutaminase
= longer lifespan, small disadvantage to normal cells

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25
Q

What is P53

A

tumor suppressor protein that regulates cell division

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26
Q

What occurs with P53 that occurs in many cancers?

A

amplified / mutated P53 regions

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27
Q

What are the 4 main phases of the cell cycle?

A

G1 (1st growth phase)
S (synthesis)
G2 (2nd growth phase)
M (mitosis)

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28
Q

What occurs in G0 phase?

A

cell no longer proliferates, only functional purpose

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29
Q

What 3 kinds of cells are in the G0 phase?

A

RBC
cardiac myocytes
neurons

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30
Q

What occurs in the S phase?

A

synthesis
DNA replication occurs

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31
Q

What occurs in the G2 phase?

A

cell prepares for mitosis by making machinery necessary for division

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32
Q

What occurs in the M phase?

A

mitosis
cell division

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33
Q

What is the primary regulatory of G1 phase?

A

Cyclin D

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34
Q

How does cyclin D regulate G1?

A

Cyclin binds to CDKs

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35
Q

What are the 4 things that regulate the cell cycle

A

regulatory proteins
cyclins
kinases
CDKs

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36
Q

CDKs are only active when ____ is expressed.

A

cyclin

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37
Q

Which phase of cell cycle can activation of growth factors only influence? Example?

A

G1
GFs upregulation of cyclin D1 in G1 phase

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38
Q

R point

A

checkpoint within cell cycle where cell cannnot be influenced by GFs

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39
Q

Which two protein families inhibit the cell cycle (suppress cycle)?

A

INK & CIP

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40
Q

What are cell cycle checkpoints? how often do they occur?

A

checkpoints to stop cell cycle if there are problems
occur during each phase

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41
Q

What mediates cell cycle checkpoints?

A

tumor suppressors

42
Q

What are two examples of tumor suppressors that mediate cell cycle?

A

P53 & PRb

43
Q

G2/M checkpoint

A

check DNA replicated, not damaged before dividing in mitosis

44
Q

M checkpoint

A

Mitotic Checkpoint Complex
(check alignment before division)

45
Q

G1/S Checkpoint

A

PRb (retinoblastoma protein) tumor suppressor present

46
Q

What tumor suppressor is activated in response to failure of the 3 critical checkpoints?

A

P53

47
Q

P53 is normally kept at (low/high) levels in the cell

A

low

48
Q

What targets p53 for degradation?

A

MDM2

49
Q

____ leads to upregulation of p53 since MDM2 cannot degrade it.

A

DNA damage

50
Q

What happens if p53 cannot fix the DNA damage?

A

apoptotic genes kill cell

51
Q

What happens to p53 in cancer?

A

misfolded/unfolded so cannot upregulate to stop damaged cells –> cancer

52
Q

What two processes is cell death important for?

A

physiological & pathological

53
Q

Why is cell death important for physiological processes?

A

maintain homeostasis
normal development

54
Q

What are the 3 forms of death?

A

apoptosis
autophagy
necrosis

55
Q

Apoptosis

A

cell “implosion”

56
Q

In apoptosis, the cell (swells/shrinks), chromatin (opens/condenses) and the membrane blebs.

A

Shrinks
Condenses

57
Q

Autophagy

A

cell “eating”
vacuolize around cell compartments

58
Q

In autophagy, chromatin (condenses/does not condense)

A

does not condense

59
Q

Necrosis

A

cell “explosion”

60
Q

Necrosis causes cell (shrinking/swelling) and membrane ____.

A

swelling
rupture

61
Q

Apoptosis is a form of (physiological/pathological) death

A

physiological

62
Q

Apoptosis is energy (dependent/independent)

A

dependent

63
Q

(T/F): Apoptosis causes an inflammatory response

A

False- vacuoles enclosed so no inflamm

64
Q

During apoptosis, the cell is broken down in vesicles called _____.

A

Apoptotic bodies

65
Q

Extrinsic Apoptotic Pathway

A

TNFa (inflammatory cytokines) bind
Caspase-8 –> Caspase-3 = apoptosis

66
Q

What inhibits the extrinsic apoptotic pathway?

A

IAPs (protein inhibitors of activated proteases) inhibit caspase so apoptosis doesn’t occur

67
Q

Intrinsic Apoptotic Pathway

A

UV/Ischemia/Hypoxia stim. cell membrane
Bax creates mitochondrial hole
Cytochrome C released
–> Caspase = apoptosis

68
Q

What inhibits the intrinsic apoptotic pathway?

A

BCL2 (which inhibits Bax) = no apoptosis

69
Q

PRRSV

A

virus affecting pigs
virus activates apoptotic proteins
affects pulmonary macrophages

70
Q

What is the primary form of pathological cell death?

A

Necrosis

71
Q

Necrosis is energy (dependent/independent)

A

independent

72
Q

Necrosis (causes inflammatory/does not cause inflammation).

A

causes inflammation

73
Q

Extrinsic Necrotic Pathway

A

TNFR –> RIPK –> RIPK3 –> MLKL
MLKL forms hole in cell membrane
water floods in = necrosis

74
Q

Intrinsic Necrotic Pathway

A

Stress affects mitochondrial pore
Pore opens –> inhibit ATP synthesis
Electrochemical gradient lost (no ATP)
mito swell + free radicals produced = necrosis

75
Q

Necrotizing Pancreatitis

A

pain/fatal disease caused by viral infections/toxins

76
Q

What protocol is used for lymphoma treatment?

A

CHOP protocol

77
Q

What is the CHOP protocol

A

rotate weeks of drug as cancer treatment

78
Q

What are two main types of vinca alkaloids?

A

vincristine
vinblastine

79
Q

What is the function of vinca alklaloids?

A

destabilize microtubules

80
Q

What are 2 mechanisms vinca alkaloids use to destabilize microtubules?

A
  1. bind to tubulin with high affinity (tubulin can’t add, microtubule not lengthening)
  2. bind to (+) end of microtubule –> shortening from treadmill effect
81
Q

MDR1

A

P-glycoprotein in cell membrane

82
Q

Function of MDR1

A

“kick-out” drug once in cell so it can’t be used

83
Q

Mechanism of MDR1

A

drug in cell –> MDR1 takes up drug –> ATP binds –> MDR1 changes conformation –> drug is “spit out”

84
Q

3 main drugs that are substrates for MDR1

A

vincristine
vinblastine
doxorubicin

85
Q

Two drugs which inhibit MDR1

A

verapamil
chloroquine

86
Q

How do verapamil/chloroquine inhibit MDR1?

A

L-type calcium channel blocker
“outcompete” vinca alkaloids against MDR cancer so they are “spit out” instead of chemotherapeutic drug (vincristine)

87
Q

3 ways to inhibit MDR1

A
  1. modify drug (so not rec by MDR1)
  2. co-administer with competitor
  3. noncompetitive inhibitior of MDR1 (overall block)
88
Q

What are two MDR proteins other than MDR1?

A

MRP1
ABCG2

89
Q

What is doxorubicin?

A

A chemotherapeutic drug

90
Q

List 3 mechanisms for cancer therapy that targets DNA

A
  1. cross-link DNA (join strands so can’t sep)
  2. intercalator (protein between nucleotides pushes apart)
  3. double-stranded break (cut in DNA)
91
Q

2 mechanisms Doxorubicin uses for cancer?

A
  1. intercalator (nuclei pushed apart)
  2. trap/inihibit DNA topoisomerases
92
Q

DNA Topoisomerases

A

enzymes that cut DNA to release tension and rebuild into correct structure

93
Q

How does doxorubicin stop DNA replication via DNA topoisomerases?

A

doxorubicin continues warped structure of DNA so topoisomerases repeat; therefore, no DNA replication can occur

94
Q

What are some phenotypic changes to the heart with doxorubicin?

A

cardiomyopathy
arrythmias
loss of myofibrils
focal necrosis & replacement fibrosis

95
Q

What does doxorubicin produce to kill cardiac monocytes?

A

free radicals

96
Q

What does doxorubicin need to produce free radicals?

A

iron

97
Q

Calpain

A

protease that degrades contractile elements in heart –> apoptosis

98
Q

What activates calpain?

A

high calcium due to leaky ryanodine receptor from doxorubicin

99
Q

______ burst in cardiac myocytes due to doxorubicin

A

Mitochondria

100
Q

Potential therapies for doxorubucin cardiotoxicity

A

antioxidants
iron chelators
ryanodine receptor stabilizers
calpain inhibitors
mitochondrial pore inhibitors

101
Q

Dystrophin function

A

used for myocyte anchoring

Cell Biology (6 decks)

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