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Cancer Drugs > Cell Biology > Flashcards

Cell Biology Flashcards

1
Q

Cell

A

Cell birth and death rate regulates the adult body size.
Adult cells do not normally proliferate unless it is healing,
Cancer occurs due to excessive cell division.
driving force of a tumor is the dev. of (4-7) genetic mutations.

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2
Q

Cell division in Cancer

A

Occurs due to mutation in GF or proteins that regulate cell division and induces uncontrolled proliferation. The cell lose their mechanism to induce apoptosis.

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3
Q

Cell Cycle G1 phase

A
  • “Gap” Prepares for DNA replication by:
    1. Making proteins
    2. Size of the cell
    3. Nutrient check
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4
Q

Cell Cycle S phase

A

“Synthesis” DNA replication and centrosome duplication

1. starts with 2n 2c ends with 2n 4c

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5
Q

Cell Cycle G2 phase

A

“Gap” replication of chromatids, and preparation for mitosis.

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6
Q

Cell Cycle M phase

A

“mitosis” cell cycle produces 2 daughter cells.
prophase, metaphase, anaphase and telophase
Has 2 most important chpts.

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7
Q

Cell Cycle G0 phase

A

Non dividing resting differentiated state

Most human cells in G0 phase

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8
Q

Chekpoint G1/S

A

Triggers replication initiation.

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9
Q

DNA damage

A

Monitors DNA throughout cycle for damage

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10
Q

G2/M

A

Prevents entry into mitosis unless all chromosomes have completely replicated their DNA.

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11
Q

Spindle Assembly Checkpoint

A

Checkpoint within the M phase that prevents entry into anaphase unless replicated chromosomes are properly attached to a spindle.

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12
Q

Chromosome Segregation

A

Prevents exit from mitosis if chromosomes are not properly segregated.

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13
Q

Go ahead or Stop Signal

A

Activators or inhibitors usually proteins

  • Go-ahead promote cell growth and division
  • Can be internal/ cytoplasmic or external (growth factors)
  • Primary mechanism of control is via phosphorylation or dephosphorylation of proteins.
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14
Q

Cyclins

A
  • Expressed a specific points in cell cycle
  • Proteins that control cell progression through cell cycle
  • Activates cyclin dependent kinases (CKD)
  • Cyclin-CDK complex trigger onset of key cycle progression and send secondary signals through cell via phosphorylation.
  • Cyclins have to detach from complex and get degredated once cell cycle is done.
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15
Q

Cyclin-CDK complex

A
  • Phosphorylates substrates to activate cell cycle specific events like initiating DNA replication
  • Has to be inactivated to prevent multiple initiation events.
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16
Q

Degradation of cyclin proteins

A

Cyclins are ubquitinated to target them for degradation.
Ubiquitin is a small protein targeting the substrate for degradation via proteasome. different Ub molecules E1, E2, E# that activates, conjugates, and ligates.

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17
Q

Proteasome (26S)

A

Large protein in the cytoplasm and nucleus. It degrades damages proteins by proteolysis. Highly regulated has two 19S caps and a 20S catalytic core.

  • 19S recognize UB proteins and transfer them to the 20S core (has to have the UB tag or it can’t enter)
  • 20S this is the site where the proteins are degraded with trypsin (hydrolyze proteins) like actions.
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18
Q

Chromosome replication

A

3 functional elements required

  1. Replication origin: DNA polymerase and other proteins initiate protein synthesis.
  2. Centromere: contristed regions required for daughter chromosomes
  3. Telomeres: at end of chromosome to prevent info loss. after each cycle the telomere shortens. Used because the lagging strand cant synthesis the whole length of the DNA.
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19
Q

Senescence

A

Telomerase is not expressed in adults, Senescence is a telomeric shortage. When there is none left the replication stops.
Cancer cells induce telomerase functions that’s how we get uncontrolled cell division.

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20
Q

Checkpoints

A

-Halt cell cycle progression to ensure that crucial events are started prior to completion of prereqs

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21
Q

DNA damage Checkpoints

A

Ensure the fidelity of genetic info by arresting the cell cycle progression and facilitation DNA repair pathways.

  • This checkpoint is in every phase. this is important because damages template and the dNTP shortage can impede proper genome duplication.
  • ATM or ATR will activate P53 to inhibit Cyclin-CDK complex stop the cycle.
22
Q

Cell growth

A

control mass of the organ and depends on

  1. cell mass: size of cell
  2. cell division: increase the number of cells
  3. cell death: decrease the number of cells
23
Q

Growth factors

A
  • extrinsic signals that control, drives and activate cell division.
  • There are 3 classes: mitogenic, growth factors and survival factors
  • Growth factors attach to receptor, tyrosine kinase sends signal, cell divides
24
Q

Mitogenic factors

A

Stimulate cell division

25
Q

Growth factors

A

Stimulate protein synthesis and membrane biogenesis

26
Q

Survival factors

A

Inhibit cell death

27
Q

Protooncognes

A
  • Act in cell proliferation paths. Needs a ligand to bind and activate the EGFR and induce cell division.
  • Most are kinases, small G proteins, and transcription factors, very controlled activity, Activating mutation will cause them to become oncogenes
28
Q

Oncogenes

A

-Mutated protooncogenes resulting from a gain of function mutation

29
Q

Mitogenic signaling pathways

A

-Extracellular proteins that stimulate cell division directly by controllinf the entry of cells into the cell cycle.

30
Q

GEF

A

-Guanine exchange factors: removes GDP and adds GTP to the molecule (activate RAS and disassociate it from SOS)

31
Q

GAP

A

GTP-ase activating protein that binds to active small G-proteins and activate the GTP-ase activity.
-GTP-ase activity is to inactivate G-protein.

32
Q

GDI

A

Guanine disassociation inhibitor: binds to some GTP bound G protein and prevent their activation (but not RAS).

33
Q

RAS pathways

A

control many different aspects of cell growth and proliferation
many downstream of RAs are protooncogenes

34
Q

MAP Kinase

A

Activated by MEK to signal transcription factors that initiate cell cycle progression.

35
Q

ERK

A

Activated by MEK to signal transcription factors, cell adhesion proteins and regulate cell growth,

36
Q

Mitogenic transcription factors

A

FOS, JUN and MYC
Activate transcription of genes essential for cell cycle progression.
-AP1 : made from combination of Fos and Jun. This is a heterodimers that can influence cyclins, GF and tumor suppressors. This factor can push the cell cycle forward.

37
Q

Tumor Suppressors

A
  • Inhibit Cell cycle progression and cell division
  • Mutations are usually recessive
  • Loss of the tumor suppressor function is carcinogenic.
  • Three classes
    1. Gatekeepers
    2. Landscapers
    3. Caretakers
38
Q

Gatekeepers

A

Act through Checkpoints

-PRB and P53

39
Q

Caretaker

A

Act in genome maintenance
ATM and ATR
BRCA 1 and 2

40
Q

Landscapers

A

Act in contact inhibition between cells (cell-cell interactions)
PTEN

41
Q

Gatekeeper PRB

A
  • Negative regulator of G1/S checkpoint

- Regulate S phase initiation

42
Q

Gatekeeper P53

A

-Multifunctional tumor suppressor protein that induce apoptosis
-Block cell progression at various points.
activated by ATM or ATR (present at all DNA damage chpts throughout the cycle)
-Induce transcription of downstream genes.

43
Q

Caretaker ATM and ATR

A
  • Acts as a DNA damage sensor and regulates P53 activity
  • Activated by Double stranded DNA damage
  • Activate DNA repair, apoptosis, and BRCA signaling

-ATR is activated by single stranded DNA damage.

44
Q

Caretakers BRCA 1

A
  • Human genes that produce tumor suppressor proteins. to help repair DNA damage and ensure stability the cell’s genetic material.
  • Stimulate homologous recombination for DS DNA damage
  • Minimize gross chromosomal rearrangement because mutations are frequent in Ds breaks
  • Leads to loss of heterozygosity (LOH)
  • Mutations lead to decrease recombinational repair. defects will increase the risk of breast cancer.
45
Q

Landscaper PTEN

A
  • Lipid phosphatase that acts in opposition to PI3K
  • Slow cell growth via dePO4lation of PIP3 to PIP2 which inhibits cell growth signals
  • PTEN is activated by paracrine signals
46
Q

Programmed cell death

A

-Apoptosis (more common), autophagy and necrosis.

47
Q

Apoptosis

A

Specialized cell death that activates Apoptosome “wheel of death”

  1. Intrinsic pathway activated by mitochondrial permeabilization
  2. Extrinsic pathways activated by TNF alpha family
48
Q

Apoptosome

A
  • Needs to be activated by cytochrome C which comes from the mitochondria.
  • CyctC binds to Apaf-1 to stimulate APaf 1- ATPase activity.
  • ATP hydrolysis will trigger the assembly of apoptosome which activates the caspase cascade that leads to the apoptotic proteolysis.
49
Q

Extrinsic Pathways

A

1-Death receptors: on cell surface activated by TNF cytokine superfamily
2-DISC: death inducing signaling complex activate procaspase protease zymogens.this activates caspase.
-Caspase: active protease that cleaves substrate proteins needed for genome integrity.

50
Q

Intrinsic Pathway

A

-Initiated by MOMP ( mitochondrial outermembrane permeabilization) which release cytC
-CytC triggers assemply of apoptosome.
-

51
Q

BCL2

A

Family proteins that regulates MOMP’s and apoptosis

  • BCL2 and BCL-XL: anti apoptotic
  • BAD and BAX: pro-apoptotic.

Cancer Drugs (3 decks)

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