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SFM Quiz 2 > Cell Cycle, Cancer, and Cell Death > Flashcards

Cell Cycle, Cancer, and Cell Death Flashcards

1
Q

What is the order of the 4 main cyclins used in the cell cycle?

A

G1: nuclear D1
S: cyclin E and cyclin A
Mitosis: cyclin B

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2
Q

What motif is necessary for the binding of cyclin to CDK?

A

PSTAIRE alpha-helix

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3
Q

How is the cycline-CDK complex inhibited/activiated?

A

It is inhibited when phosphorylated at 2 specific sites. It is activated when it is phosphorylated at another site.

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4
Q

What is the role of Cdc25?

A

It is a protein phosphatase that activates the cyclin-CDK complex

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5
Q

What are the cyclin-dependent kinases for cyclin A?

A

CDK1 and CDK2

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6
Q

What is the cyclin-dependent kinase for cyclin B?

A

CDK1

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7
Q

What is the cyclin-dependent kinase for cyclin E?

A

CDK2

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8
Q

What are the cyclin-dependent kinases for cyclin D?

A

CDK4 and CDK6

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9
Q

What is the difference between the mechanism of INK4 vs p27?

A

IDK4: binds to CDK, blocking cyclin from binding. Or, it can bind to the cyclin-CDK complex, interfering with ATP hydrolysis.
p27: binds to cyclin-CDK complex, blocking ATP from binding.

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10
Q

What are the substrates for CKIs p21 and p27?

A

Most cyclin-CDK complexes

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11
Q

What are the substrates for INK4 p16?

A

CDK4 and CDK6

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12
Q

Explain how the Ras pathway is activated.

A

Membrane receptor becomes active by mitogen, which connects to and activates Ras on the cytosolic side by binding GTP. Ras activates MAP kinase, which activates a cascade than leads to the production of Myc. Myc is a transcription factor that eventually leads to cell entry into S Phase.

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13
Q

What is the restriction point and how does it occur?

A

It is the point where cells commit to divide. Occurs once the D-CDK4/6 is formed, phosphorylating pRb. This signals E-CDK2 to hyperphosphorylate pRb. This leads to pRb dissociating from E2F. E2F is a transcription factor that increases the production of E-CDK2 and itself, further amplifying its activity.

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14
Q

What is the purpose of A-CDK2?

A

It stabilizes the prereplication complex during S phase.

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15
Q

What is the purpose of B-CDK1?

A

To initiate spindle assembly during mitosis. Degraded by activated anaphase promoting complex (APC).

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16
Q

Describe the slower G1 checkpoint pathway.

A

ATM is activated following damage. This leads to the stabilization of p53 which transcriptionally upregulates p21. p21 then binds and inhibits cyclin-CDK complexes.

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17
Q

Describe the faster G1 checkpoint pathway.

A

ATM is activated following damage. This leads to activation of Chk2. Chk2 inactivates Cdc25, so the inhibitory phosphates of E-CDK2 cannot be removed.

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18
Q

What is the significance the ARP/p16 G1 checkpoint?

A

If activated, the cell will likely never undergo cell division.

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19
Q

What is the difference between the G1 and G2 checkpoints?

A

G2 has similar slow and fast pathways, expect B-CDK1 is the only complex that is inhibited.

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20
Q

What are the stages of Carcinogenesis?

A

Initiation: genotoxic event (change in DNA sequence)
Promotion: epigenetic event (change in gene regulation)
Progression: clastogenic events and others (further changes in karyotype)

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21
Q

What is the difference in threshold for mutations in oncogenes vs tumor suppressor genes?

A

Oncogenes: Only one out of the two alleles needs to be mutated to caused abnormal cell growth (dominant, gain of function).
Tumor suppressors: Needs both alleles to be mutated to cause abnormal cell growth (recessive, loss of function).

22
Q

What are the 3 forms of oncogenes?

A
  1. Cellular proto-oncogenes that have been captured by retroviruses.
  2. Virus-specific genes that behave like cellular proto-oncogenes that have been mutated.
  3. Cellular proto-oncogenes that have been mutated.
23
Q

How can transducing viruses lead to cancer?

A

By incorporating cellular oncogene carried by retrovirus.

24
Q

How can non-transducing viruses lead to cancer?

A

A viral promoter or enhancer is added to a cellular oncogene, causing overproduction.

25
Q

How can non-transducing long latency viruses lead to cancer?

A

Retroviral transactivation protein disrupts normal regulation of cellular transcription.

26
Q

How can retroviruses that contain an envelope that signals cause cancer?

A

Inappropriate cellular signaling resulting from viral envelope/cell receptor interactions.

27
Q

What kind of viruses can cause anogenital cancers and skin cancers?

A

Papillomaviruses

28
Q

What are the 3 main components of the tumor microenvironment?

A
  1. Cellular components (non-cancerous cells) such as immune cells, fibroblasts, and blood vessels.
  2. Secretory factors such as signaling molecules, growth factors, inflammatory factors, and enzymes.
  3. Extracellular matrix which contains fibrous proteins and Proteoglycans, providing structural support for the multicellular environment.
29
Q

What is a desmoplastic reaction?

A

A reaction that is associated with some tumors and is characterized by the pervasive growth of dense fibrous tissue around the tumor.

30
Q

What is paracrine signaling?

A

A communication in which a cell produces a signal to induce changes in nearby cells, altering behavior of those cells.

31
Q

What are the 4 main types of cancer treatments?

A

Surgery, radiation therapy, chemotherapy, and immunotherapy

32
Q

How do Alkylating agents work?

A

They denature certain macromolecules such as DNA macromolecules.

33
Q

How do Intercalating agents work?

A

They interact with DNA and intercalate between two bases, inducing a structural change. This change activats cleaving agents that break DNA.

34
Q

How do Antimetabolites work?

A

They can be structural analogies or purines or pyrimidines, blocking synthesis of corresponding bases.

35
Q

How do Mitostatic agents work?

A

They inhibit tubulin synthesis so the cell cannot make the microtubules needed for mitosis.

36
Q

How do Platinum derivatives work?

A

They block synthesis by binding to DNA.

37
Q

What is the main mechanism of cell in cancers?

A

Mitotic catastrophe

38
Q

What is necrosis and how is it characterized?

A

Uncontrolled cell death. Characterized by increased swelling and eventual rupture of cells. Leads to inflammation. Occurs in all cell types.

39
Q

Describe one of the ways necrosis is induced.

A

Activation of RIP protein when under stress, leads to production of ROS that damage mitochondria, causing ATP depletion.

40
Q

What is apoptosis and how is it characterized?

A

Programed cell death. Characterized by membrane blebbing and fragmentation. Does not cause inflammation. Occurs in hematopoietic (RBC stem cells) only.

41
Q

What are the 4 main triggers of apoptosis?

A

DNA damage, death receptors signaling, cell membranes (sphingomyelin), and mitochondrial damage.

42
Q

Describe how p53 can induce apoptosis.

A

DNA damage activates ATM then p53. p53 then activates BH3 which removes Bcl-2 from the outer mitochondrial membrane. This allows Bax and Bac to form pores in the membrane, allowing cytochrome c to be release and trigger apoptosis cascade.

43
Q

Describe how Caspase-8 can induce apoptosis.

A

Membrane receptor releases Caspase-8 in response to a ligand. Caspase-8 then activates Caspase-3, which is a protease than induces cell death. Caspase-8 can also activate Bid and induce the Bax/Bak pathway.

44
Q

What is Autophagy and how is it characterized?

A

“Self-eating” and “Recycling.” Characterized by membrane blebbing, accumulation of two-membrane autophagic vacuoles. Does not cause inflammation. Occurs in all cell types.

45
Q

What are two important proteins involved in the autophagy cascade?

A

Beclin-1 and LC3

46
Q

What is mitotic catastrophe and how is it characterized?

A

Cell death caused by aberrant mitosis. Characterized by larger cytoplasm, micronucleation, and multinucleation. Does not cause inflammation. Occurs in most dividing cells.

47
Q

What are the 3 mechanisms that can induce mitotic catastrophe?

A
  1. Defects in cell cycle checkpoints
  2. Hyperamplification of centrosomes
  3. Caspase-2 activation during metaphase
48
Q

What are the 3 possible fates for aberrant mitosis?

A
  1. Mitotic death, die without exiting mitosis.
  2. Delayed cell death, proceed to G1 and continue division for many cycles then undergo death.
  3. Senescence, exit mitosis and undergo permanent G1 arrest.
49
Q

What is senescence and how is it characterized?

A

Permanent cell cycle arrest. Characterized by flatted and granulated cytoplasm. Looks like a “fried egg.” Leads to inflammation. Occurs in all cell types.

50
Q

What 2 pathways can lead to senescence?

A
  1. p53-p21

2. P16-Rb

SFM Quiz 2 (15 decks)

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