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Molecular Test III > Lecture 24 Apoptosis and Cancer I > Flashcards

Lecture 24 Apoptosis and Cancer I Flashcards

0
Q

What are the phenotypes of apoptosis?

A

Overall shrinkage in vol of cell and its nucleus
Loss of adhesion to neighboring cells
Formation of blebs on surface
DNA fragmentation
Cytoskeleton collapses
Nuclear envelope disassembles
Rapid engulfment of dying cell by phagocytosis
Cytochrome C released from mitochondria is another marker

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1
Q

What is apoptosis?

A

Cells undergoing cell death under physiological conditions
Clean way of dying compared to necrosis
It is a programmed cell death
Most common cell death
Done to minimize spread of damage and/or inflammation
Cells shrink and condense and contents never spill out

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2
Q

Caspases:

A

Activation of caspases is a key event in apoptosis
=Cystein ASPartyl specific proteASE
Has a cysteine in active site
Targets proteins and cleaves them in their sequence where an aspartic aa residue occurs

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3
Q

Procaspase:

A

Inactive precursor form of caspases
Becomes activated by protease cleavage
Procaspases cleaved at specific sites to form a large and small subunit which forms a heterodimer

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4
Q

Initiator caspases:

A 
Initiates apoptosis (includes caspase-8 and caspase-9)
These activate executioner caspases
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5
Q

Executioner caspases:

A 
Destroys actual targets
Executes apoptosis
Caspase-3
Cleaves downstream proteins
Cleaves inactive endonuclease
Targets cytoskeleton
Attacks cell adhesion proteins-cells roll up into a ball

*CASPASE CASCADE IS IRREVERSIBLE

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6
Q

How are initiator caspases activated?

A

they auto-activate themselves

The machinery for apoptosis is always in place

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7
Q

Describe internal pathway

A

Internal stimuli: abnormalities in DNA

Mitochondrial dependent

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8
Q

Describe external pathway

A

External stimuli: removal for survival factors and proteins of tumor necrosis factor family
Mitochondrial independent
Extracellular signals bind to death receptors and trigger pathway

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9
Q

What are death receptors

A 
Transmembrane proteins with 3 domains
-extracellular binding domain
-single transmembrane domain
-intracellular death domain
Receptors are homotrimers: three proteins of same type
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10
Q

Describe the Extrinsic pathway cascade

A

Fas binds to Fas death receptor
Adaptor proteins recruited: FADD and procaspase-8 with death effector domain
Activates caspase-8 or -10 (forms DISC)
Activates downstream executioner caspases - caspase-3

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11
Q

What are inhibitory proteins for extrinsic pathway?

A

Decoy receptors: have ligand binding domain but no death domain, can bind death ligand but does not activate pathway

FLIP: protein resembling initiator procaspase with no proteolytic domain; competitive inhibitor against procasp-8 and -10: prevents apoptosis

Act as sponges

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12
Q

Describe the intrinsic pathway cascade

A

Cytochrome C is released from mitochondria
Binds to Apaf1
Apaf1 forms apoptosome which activates casp-9
Casp-9 activates downstream executioner casps - casp - 3

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13
Q

What controls the release of cytoc C into cytosol?

A

Bcl2

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14
Q

What are the two types of Bcl proteins?

A

Pro-apoptotic and Anti-apoptotic

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15
Q

Describe anti-apoptotic protein Bcl2

A

Has 4 distinctive domains: called Bcl homology domains or BH

Blocks release of cytoc C

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16
Q

Describe pro-apoptotic proteins

A

BH123 + BH-3 only protein

Promotes release of CytocC

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17
Q

What is the function of BH123 protein?

A

It is a pro-apoptotic Bcl protein that once activated by stimulus, it forms an aggregation in mitochondrial outer membrane and induce release of cytoc C

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18
Q

What is the role of Bcl2 and Bcl-XL?

A

They are both BH1234
Anti-apoptotic Bcl protein that is mainly located on cytosolic surface of outer mitochondrial membrane
Prevent apoptosis by binding to pro-apoptotic proteins and prevent aggregation into active form

19
Q

What is the role of BH3 - only protein?

A

pro-apoptotic
An activated BH3-only protein is cytosolic and translocates to mitochondria after apoptotic signal activates it
Inhibits anti-apoptotic Bcl2 protein from inhibiting aggregation to release cytochrome C

20
Q

IAPs:

A

Inhibitors of apoptosis
Bind and inhibit caspases
Some add ubiquitin to caspases to mark for destruction
IAPs block apoptosis by binding to caspases
IAPs are there for when initiator caspases spontaneously activate but the cell does not need to die

21
Q

If there is apoptotic stimuli or apoptosis signals, how are IAPs surpassed?

A

There is a release of anti-IAPs when apoptosis needs to occur from the mitochondria to block activity of IAPs
Executioner caspases can therefore be activated.

22
Q

How is cancer caused by excess Bcl2?

A

if there is always inhibition of apoptosis, then DNA-damaged cells will not be programmed for cell death but can go on to cause cancer

23
Q

How does p53 mutation cause cancer

A

Mutated p53 can no longer cause cell cycle arrest
No longer promotes apoptosis
Cells with DNA damage sticks around

24
Q

What is cancer?

A

A disease in which an individual mutant clone of cells begin by prospering at the expense of its neighbor cells
Cells growing of control - dont need signals to grow and are self-sustaining
Release autocrine growth factor signals

25
Q

What is cell growth controlled by?

A

Growth factors

-those produced by other cells stimulate target cells to divide

26
Q

What small protein growth factor is produced by kidney when RBC count is low?

A

Erythropoeitin

Stimulates bone marrow to produce more RBCs

27
Q

What are two heritable properties of cancer cells?

A

Reproduce in defiance of normal restraints on cell division and cell growth
Invade areas normally reserved for other cells

28
Q

How does cancer kill?

A

As a tumor grows and spreads, it squeezes or destroys blood vessels, nerves, until an organ can no longer do its job and death results

29
Q

What is a benign tumor?

A

an abnormal cell that grows and proliferates out of control will give rise to a tumor or neoplastic growth. If neoplastic cells do not become invasive then tumor is benign and can be surgically removed
Benign =x cancer

30
Q

Carcinomas:

A

From epithelial cells - most common

31
Q

Sarcomas:

A

From connective tissue and muscle tissue

32
Q

Leukemias and lymphomas come from what?

A

White blood cells and their precursors

33
Q

Adenoma:

A

benign epithelial tumor with glandular organization

34
Q

A malignat tumor of the same type as adenoma is called what?

A

adenocarcinoma

35
Q

Basal-cell carcinoma :

A

keratinocyte stem cell in skin

Rarely metastasize

36
Q

Melanoma:

A

pigment cells in skin

Malignant melanomas metastasize

37
Q

What is metastases?

A

Invasiveness is property of cancer
Cancer cells break loose, enter into blood or lymph, travel to new areas and form secondary tumors
Hard for a tumor to metastasize because only 1/1000 invading cells survive

38
Q

Cancer cell contain what kind of mutations?

A

somatic

39
Q

Carcinogenesis (generation of cancer) is linked to what?

A

mutagenesis (mutant change in DNA)

40
Q

What are two types of carcinogens?

A

Chemical carcinogens and radiation

41
Q

Cancerous growth depends on defective apoptosis or growth. How is obesity related to incidence of cancer?

A

more cells/ more chances of mutations

42
Q

What is angiogenesis? How is it related to tumors?

A

Angiogenesis is the formation of new blood vessels from pre-existing blood vessels
Tumors must get oxygen and nutrients like normal cells
Release factor to induce new blood vessel formation
Target of cancer therapy

43
Q

Tumors are made up of many cells. name them

A

Cancer cells, fibroblasts and stroma: supportive connective tissue Endothelial cells-blood supply

44
Q

What are environmental causes that can lead to cancer?

A

Diet
Carcinogens (chemicals, UV light, X-rays)
Viruses and infections (AIDS, Ulcers, helicobacter pylori)
Tobacco-most important environmental cause of cancer

Molecular Test III (7 decks)

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