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Biochem 1502 > Cell Cycle and Cancer > Flashcards

Cell Cycle and Cancer Flashcards

1
Q

G1 checkpoint checks for

A

Favorable environment and DNA damage

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2
Q

G2 checkpoint checks for

A

DNA replication complete, chromosomes intact

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3
Q

What cells are permanently in G0 and are unable to replicate

A

neurons

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4
Q

Senescence

A

decrease in the proliferative capacity with age, irreversible

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5
Q

If a cell can be activated by external agents to enter cell cycle, it is called

A

quiescent

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6
Q

A cell that has not committed to cell cycle “specialized resting state” is known to be in…

A

G0

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7
Q

chemotherapeutic agents target rapidly dividing cells and are only effective on tumors with a high percentage of replicating cells

A

cell cycle specific

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8
Q

Which chemotherapeutic drugs are useful against low percentage replicating cells?

A

b. Cell cycle non-specific

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9
Q

3 classes of cell cycle specific chemotherapeutics

A

antimetabolites, antibiotics, mitotic spindle poisons

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10
Q

Antimetabolites

A

inhibit purine or pyrimidine precursors or compete with them for incorporation into DNA/RNA. Effects S-PHASE

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11
Q

Examples of Antimetabolites

A

Methotrexate, 5-flurouracil

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12
Q

Methotrexate

A

inhibits thymidine synthesis by inhibiting regeneration of tetra-folate for normal folate metabolism – starving cells of folate

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13
Q
  1. 5-Flurouracil
A

irreversibly binds dUMP preventing synthesis of Thymidylate and preventing DNA biosynthesis

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14
Q

Anticancer antibiotics

A

Cell cycle specific and non-specific, but Bleomycin causes cells to accumulate in G2 PHASE

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15
Q

Examples of Anticancer antibiotic

A

Bleomycin (G2 PHASE SECIFIC)

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16
Q

Examples of Mitotic Spindle Poisons

A

Vincristine, Vinblastine (Vinca alkaloids), and Taxol

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17
Q

Mitotic Spindle Poisons

A

M-PHASE SPECIFIC: (Vinca alkaloids) block mitosis by binding to tubulin, disrupting the spindle apparatus and causing depolymerization. Taxol causes stabalization of MTs and prevents disassembly

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18
Q

Taxol

A

Mitotic Spindle Poisons - causes stabalization of MTs and prevents disassembly

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19
Q

Vincristine, Vinblastine (Vinca alkaloids)

A

Mitotic Spindle Poisons - block mitosis by binding to tubulin, disrupting the spindle apparatus and causing depolymerization

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20
Q

What non-malignant cells are effects by chemotherapy?

A

hair follicles, none marrow, GI tract epithelium

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21
Q

2 types of cell cycle regulation

A

cascade of protein phosphorylation (cyclin-CDK), checkpoints

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22
Q

Cyclin

A

cell cycle regulators that cycle due to synthesis and degradation during the cell cycle

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23
Q

What causes degradation of cyclin?

A

ubiquitin tagged proteosomal pathway

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24
Q

CDK

A

constant concentration, but enzyme activity changes throughout cell cycle

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25
What 4 things regulate CDK
a. Association with cyclins b. Phosphorylation at stimulatory sites c. Phosphorylation at inhibitory sites d. Binding to CDK inhibitors
26
Association of CDK-cyclin complex causes
phosphorylation of the CDK protein which is then active to add phosphate groups to its target proteins
27
CDK necessary for S-phase transition
CDK2, triggers DNA replication machinery
28
CDK necessary for M phase transition
CDK1; triggers mitosis machinery, MTs
29
What Cyclin-CDK complex is required for passage through R point?
Cyclin D + CDK4/6
30
What Cyclin-CDK complex is required for G1/S-phase transition?
Cyclin E + CDK2
31
What Cyclin-CDK complex is required for S/G2-phase transition?
Cyclin A + CDK2/1
32
What Cyclin-CDK complex is required for G2/M-phase transition?
Cyclin B + CDK1
33
Retinoblastoma
regulates G1 checkpoint and inhibits cell cycle
34
In early G1, Rb is...
underphosphorylated, which allows it to bind and "hold back" TFs required for G1/S transition
35
Increasing concentration of D/CDK4-6 causes..
Hyperphosphorylation of Rb, resulting in release of TFs and activation of genes necessary for S-phase
36
What activates Cyclin D1?
MAP-kinase cascade by growth factors
37
What TFs ae inhibited by Rb?
E2F and DP1
38
p53
tumor suppressor gene that detects DNA damage and determines progression of cell cycle
39
p53 is a TF for what gene?
it can turn on transcription of CDK inhibitor p21 (CIP) which will halt cell cycle in G1 phase to allow time for DNA damage repair
40
What does p53 do if damage is irreparable?
triggers apoptosis
41
3 p53 functions:
regulates genes involved in cell cycle control, arrest the cell during DNA damage, and commits a cell to apoptosis if necessary
42
tumor suppressor genes
proteins involved in checkpoint control
43
Most common mutation in cancer
p53
44
HPV 16 and 18 and their viral proteins E6 and E7
Bind p53 and Rb respectively and cause loss of function
45
Mutations in p53 commonly occur in which domain?
The DNA binding domain, meaning it cannot bind to the promotor of CDKi/p21/CIP
46
During apoptosis, cleavage of what proteins allows cell to begin shrinking?
Lamins and actin filaments
47
During apoptosis, the cell shrinks, chromatin breaks down and nucleus and cell fragment and are removed by?
Macrophages
48
What is done by the cell to promote phagocytosis by macrophages?
translocation of phosphotidylserine from the inside of the cell to the outer surface
49
Apoptosis in hematopoiesis
EPO not only promotes cell division, but it also inhibits apoptosis
50
How does EPO inhibit apoptosis?
EPO binds its receptor (tyrosine kinase) on erythroid precursors and induces anti apoptotic molecule (Bcl-XL)
51
Apoptosis and estrogen
Estrogen causes apoptosis of osteoclasts to prevent bone resorption, estrogen deprivation in post-menopausal women results in osteoporosis
52
Apoptosis in aging
Deregulated apoptosis - apoptosis of irreplaceable cells (neurons, cardiac myocytes), decreased apoptosis of damaged or senescent cells
53
How can cancer cells be resistance to chemotherapy
inability to activate apoptosis machinery
54
CNS during acute ischemia or traumatic injury would result in
necrotic death at the site of injury, apoptosis may occur at a certain distance from the injury site
55
Chronic neurodegenerative diseases would result in
apoptosis
56
Neurodegenerative disease list
Huntingtons, Alzheimers, Parkinsons- chronic stroke, brain trauma, spinal cord injury - acute
57
Would the presence of cytokines cause apoptosis?
No
58
Would the presence of oxidation cause apoptosis?
Yes
59
Activation of apoptosis occurs when
a signal is generated from within the cell, substances bind receptors on the cell surface (death receptors)
60
Which two families of proteins mediate apoptosis?
Caspases and BCl2
61
Caspases are
cysteine aspartate proteases that exist as a proenzyme
62
BCl2 are
pro-survival and pro-death factors
63
How do caspases work?
they have a proteolytic cysteine that cleaves proteins at an aspartate once signals are received and enzymatic cleavage activates the enzyme
64
Initiator caspase
cleave and activate proteins in the caspase cascade to trigger the onset of apoptosis
65
Effector Caspase
cleave and destroy critical components of the cell
66
BCL-2 family members that are pro-survival
BCL2 and BCL-XL
67
BCL2 family members that are pro-death
BAX, BAD, BID, BAK
68
The ratio of what determines the cell's fate
Pro-death and pro-survival BCL2 proteins
69
In neurodegenerative diseases apoptosis is inappropriately
ACTIVE
70
In cancer, apoptosis is
DECREASED
71
Cytochrome c
mediates apoptosis via release fro the mitochondria
72
BH-3
A unique domain on PRO-DEATH BCL2 proteins that binds to and INHIBITS pro-survival proteins
73
BCL-2
located on mitochondrial membrane, bound to Apaf-1
74
What happens when BCL2 pro death proteins recognize cell stress
They bind BCL-2, causing mitochondrial membrane to depolarize and form pores which allow cytochrom c and smac/diable to enter the cytosol
75
Anti-apoptic proteins
located within the mitochondria and function to keep the mitochondrial membrane intact
76
Pro-apoptotic proteins
located in the cytosol and detect cell stress
77
Cytochrome C
located within the Mitochondrial inter membrane space, released when pro-apoptotic proteins bind BCL-2, causes activation of caspase 9
78
When the pro-apoptotic signals bind BCL2, what happend to the mitochondrial membrane
it becomes depolarized and pores result, which allow release of cytochrome c and SMAC/DIABLo
79
Apaf-1
generally bound to mitochondrail membrane with BCL-2, but when pro-death proteins bind and pores form, it is released and works with cytochrome c to activate caspase 9
80
apoptosome
Cytochrome C + Apaf-1, molecules of caspase 9 form a multiprotein complex
81
Caspase 9
stress pathway; activates other caspases and leads to proteolytic activity to degrade structural proteins and DNA
82
Smac/DIABLO
Also released from mitochondria when pores form, they inactivate a group of anti-apoptotic proteins (IAPs)
83
Tumor necrosis factor
integral membrane receptor that binds TNF-alpha and activates the death receptor (extrinsic apoptotic pathway)
84
Fas
integral membrane receptor that binds FASL and activates the death receptor (extrinsic apoptotic pathway)
85
TNF and Fas activate
death-signaling complex and activation of Caspase 8, which activates other caspases and results in phagocytosis of the cell
86
Caspases 3, 6, 7
FINAL EXECUTIONERS, activate proteases and DNases
87
Caspases activate
DNases (which work at coils, defined length fragments), proteases that breakdowm structural proteins (laminas), and INHIBIT DNA repair enzymes
88
p53 and apoptosis
Increases BAX, increases Fas receptor, and reduces levels of growth factors (IGFBP3)
89
Nucleosomal fragments
result from DNase activity since DNases work between the nucleosome complexes

Biochem 1502 (14 decks)

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