control of the cell cycle

Checkpoints

points where the cell is checked for further processes to transition to one phase to another

G1/S checkpoint

growth factors will bind to TKR and create a phosphorylation cascade. the final kinase will enter the nucleus and phosphorylate Rb (Retinoblastoma Protein) which will release the transcription factor: E2F. E2F will catalyze the transcription of DNA to mRNA. mRNA will translate into cyclin. cyclin will bind to CDK, which will activate the CDK and phosphorylate proteins that will move cells from G1 to S phase. After cells move from g1 to s phase, cyclin will be destroyed and kinase will be inactive

PDGF (platelet derived growth factor)

when tissues are injured, blood clots form from platelets. platelets will release PDGF and will trigger nearby cells to divide and heal the wound

G2/M checkpoint

MPF (mitosis promoting factor) will phosphorylate proteins that’s required for mitosis such as protease which will destroy the cohesins that join the sister chromatids together

Spindle Checkpoint

APC (anaphase promoting complex) will remove all inhibitors for proteases which will destroy/breakdown cohesins that join the sister chromatids together, allowing them to separate

Spindle fibers ensure what

that all chromosomes are attached to spindle fibers and are present at metaphase

Density Dependent Inhibition

crowing cells will stop dividing due to a decrease in supply of growth factors and essential nutrients

Anchorage Dependence

to divide, cells will attach to substratum (base) such as the inside of a culture jar

Cancer

uncontrollable cell division

Causes for cancer

1. mutation in gens that control the cell cycle

2. Mutation in the tumor

3. Viruses

4. Chemicals

Mutations in the genes that control the cell cycle

proto-oncogenes and tumor-suppressing gene

Proto-Oncogene

codes for growth factor and growth factor of receptors

what happens in proto-oncogene?

mutations in this gene is called oncogene in which it codes for faulty receptors that stimulate cell division without the presence of growth factors

tumor-suppressing gene has…

p53 and p21

p53 & p21

a tumor-suppressing gene that codes for p53 protein. this protein will check for dna damages. if it comes across one, it will stop cell division at g1 checkpoint and p53 will transcribe to p21. p21 protein will bind to cyclin to prevent it from binding to CDK, which blocks cell cycle at G1 checkpoint. after the cell stops, p53 gene will initiate the transcription of repair enzymes

If DNA is significantly damaged…

p53 will induce apoptosis to remove the damage cell

Mutation in the tumor

suppressor gene that blocks the transcription of telomerase

telomerase

an enzyme that add telomeres to the end of chromosomes

telomeres

short sequence of nucleotides TTAGGG repeated numerous times on the ends of chromosomes for protection

what happens in telomeres

telomeres segments are lost everytime a cell divides, eventually cell line (base) is no longer able to divide. in healthy cells, a tumor suppressor gene inhibits the production of the enzyme telomerase that builds telomeric segments

why do cancer cells avoid telomeric shortening?

the gene is mutated so it will continuously transcribe mRNA to create active telomerase

example of Viruses

papilloma virus which cause cervical chaser and RSV, which is associated with chicken sarcoma

RSV

an RNA virus called retrovirus which produce by transcribing its RNA into DNA and then inserting the DNA into the host cellular chromosome. these viruses have enzymes called reverse transcriptase that convert RNA into DNA

how do viral genes cause cancer?

SCR genes. the cancer result from the activity of these genes which code for faulty receptors stimulating cell division in the absence of growth factors

Chemicals

cause mutation in DN which lead to cancer. example: benzene, abestos, arsenic