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Biology 465 > Lecture 10 - 12 > Flashcards

Lecture 10 - 12 Flashcards

1
Q

What are the two kinds of inflammation?

A

Acute or chronic

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2
Q

What occurs during the resolution of an inflammation?

A

The levels of proinflammatory mediators and infiltrated immune cells decline

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3
Q

What is chronic inflammation?

A

It is caused by infectious or autoimmune diseases. It is a prolonged abnormal immune response that is not resolved by the normal feedback mechanisms
- associated with the development of 30% of malignancies worldwide

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4
Q

What is chronic inflammation thought to promote in tumours?

A
  • tumour initiation, progression and metastasis by providing a tumour-supporting microenvironment
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5
Q

What is an important concept about metastatic spread?

A

Metastatic spread is responsible for ~90% of cancer-related mortality

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6
Q

What is responsible for metastatic spread?

A

Changes in genes controlling cell-cell and cell matrix interactions (eg., E-cadherin, integrins)

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7
Q

What is E-cadherin?

A

A transmembrane protein that mediates cell-cell interactions

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8
Q

What is tumour progression associated with?

A
  • the loss of E-cadherin function and the transition to a more motile and invasive phenotype
  • cell pseudopod movement
  • requires the coordinated regulation of both E-cadherin-mediated cell-cell adhesions and integrin-mediated adhesions that contact the surrounding ECM
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9
Q

How is the regulation of E-cadherin and integrin dynamic?

A

Cells respond to external cues from the tumour microenvironment that regulate polarity, directional migration and invasion

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10
Q

How would a loss of cadherin junction occur?

A

E-cadherins are supported by p120, alpha and beta catenin. If any of the catenins lose their function, then there is a loss of cadherin junction

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11
Q

How does cadherin junctions protect the cell from cancer?

A
  • protects from growth factors effecting the cell due to contact inhibition
  • stays differentiated
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12
Q

What are integrins?

A

Heterodimeric cell-surface glycoproteins that serve to mediate cell-ECM interactions
- like cues from the extracellular environment to the actin cytoskeleton

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13
Q

What is EMT?

A
  • epithelial to mesenchymal transition (EMT)
  • a process normally involved in embryonic morphogenesis and wound healing/repair
  • cells acquire ability to invade, resist apoptosis and to disseminate
  • controlled by several TF (eg., Slug)
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14
Q

What is Slug?

A
  • a zinc finger transcriptional repressor which down-regulates expression of E-cadherin
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15
Q

What does Slug do the cell?

A
  • Causes a loss of adheren junctions and expression of matrix degrading enzymes, increased motility and resistance to apoptosis
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16
Q

What occurs if Slug expression was increased?

A

It induces tightly bound epithelial cells to break into a loose mesenchymal phenotype and maintenance of this phenotype enables metastasis of tumour cells

17
Q

How was it determined that Slug suppresses E-cadherin transcription?

A

On a western blot:

  • cells that had been less invasive in nature had large amounts of E-cadherin and little to no expression of Slug
  • in more invasive cells, there was no E-cadherin and large amounts of Slug expressed
18
Q

What three changes occur during tissue invasion and metastasis?

A
  1. Changes in genes controlling cell-cell and cell matrix interactions
  2. Upregulation of protease genes (eg. matrix metalloproteases)
  3. Down-regulation of protease inhibitors
19
Q

Is genomic instability a product of being cancerous or a cause?

A
  • cancer arises from the accumulation of multiple mutations in the same cell
  • tumour cells must acquire an increased mutability
  • results in the loss of p53 and DNA repair genes
20
Q

What is the role of MSH2 and MSH6?

A
  • MSH2: the protein that recognizes the mismatch

- MSH6: the protein that performs the repairs

21
Q

What occurs if there are mutations in MSH2 and 6 that results in down regulation?

A

It will result in the loss of fidelity that is identified in cancer

22
Q

What occurs if there is a double stranded DNA break repair?

A
  • the loss is lethal to a cell
  • apoptosis or necrosis
  • chromosomal abnormalities
23
Q

What are important proteins that if mutated can contribute to cancer?

A

Rad 51 (& 50), ATM, BRCA1 and BRCA2

24
Q

How would a mutated ATM (eg. down-regulated)cause cancer?

A
  • lack of ATM would decrease the phosphorylation of p53

- p53 would be unable to act on p21, Gadd45 and 14-3-3 which would result in S phase and M phase occurring.

25
Q

What are the roles of BRCA1 and 2?

A

They act as scaffolds in assembling repair machinery

26
Q

What are the differences between BRCA1 &2?

A
  • BRCA1 is a large protein that allows other proteins to attach (including BRCA2). If knocked out, it is lethal as it is needed for DNA repair
  • Rad50 is bound to BRCA1 and Rad51 is bound to BRCA2
27
Q

What are the roles of Rad 50 & 51?

A
  • both involved in double stranded DNA repair
  • both allow other proteins to bind to it
  • Rad50 binds to BRCA1
  • Rad51 binds to BRCA2
28
Q

Do normal cells prefer glycolysis or the citric acid cycle? What about cancer cells?

A
  • normal tissues tend to use the citric acid cycle in aerobic conditions (90%), if undergoing hypoxia in anaerobic conditions then they use glycolysis (10%)
  • cancer cells are more prone to using glycolysis despite high oxygen levels
29
Q

What is the Warburg Effect?

A

Even in the presence of oxygen, cancer cells reprogram their energy metabolism to preferentially use glycolysis

30
Q

What is the mechanism of the Warburg Effect?

A
  • Ras is activated oncogenically
  • With PTEN, Ras activates HIF1-alpha
  • HIF1-beta binds to HIF1-alpha which allows them to enter the nucleus as a TF
  • Glut1 is expressed
31
Q

How do HIF1-alpha levels decrease?

A
  • HIF1-alpha can be hydroxylated
  • once hydroxylated, VHL (Von Hippel-Lindau factor (E3)) can bind HIF1-alpha
  • results in the ubiquination of the complex
  • negative regulation
32
Q

If mitochondrial activity was decreased, how would this help a tumour?

A
  • less HIF1-alpha available

- can not induce apoptosis

33
Q

What is PET Scanning?

A
  • Positron Emission Tomography (18 Fluorodeoxyglucose tracer)
  • utilizes the reliance of cancer cells on glycolysis (glucose uptake) to generate images of the cancer
34
Q

Why do cancers make the switch to glycolysis? Is there an advantage?

A
  1. One possible advantage is the glycolysis leads to an increase in anabolic substrates for lipid, protein synthesis, etc.
  2. Decreases the reliance on the mitochondria
35
Q

Cancer cell growth is limited to areas surrounding blood vessels, What is the result of this?

A
  • decrease of oxygen consumption
  • increase in growth radius
  • reduced use for mitochondrial function to conserve oxygen located in cells not near the blood vessel
36
Q

How does the tumour microenvironment effect (fibroblast, endothelial cell and immune cells) the acquired traits?

A
  • fibroblasts contribute to the support that allows cancer cells to grow large
  • endothelial cells, stimulated by VEGF, allows cancer cells to enter the blood stream
  • immune cells with their surveying and editing has allowed the cancer cell to avoid the editing and will seed eslewhere

Biology 465 (15 decks)

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