7. Proto-oncogenes and Oncogenes
Summary
TLDRThis video for medical students delves into the molecular basis of cancer, focusing on proto-oncogenes and oncogenes. It explains how mutations in DNA can lead to faulty proteins and cancer's hallmarks. Proto-oncogenes are genes that encourage cell division, and when mutated into oncogenes, they promote uncontrolled cell growth. The video uses the car analogy, comparing tumor suppressor genes to brakes and oncogenes to an accelerator, highlighting the difference between loss of function in tumor suppressors and gain of function in oncogenes, which only requires one mutation to lead to cancer.
Takeaways
- 𧬠Cancer development is linked to DNA mutations that result in faulty proteins and the hallmarks of cancer.
- π Proto-oncogenes are genes that normally encourage cell division; when mutated, they become oncogenes.
- π Tumor suppressor genes act as 'brakes' to control cell cycle progression, while oncogenes act as 'accelerators'.
- π± A gain in function of proto-oncogenes, turning them into oncogenes, leads to uncontrolled cell division and cancer growth.
- π The RAS gene is the most commonly mutated oncogene in human cancers, playing a critical role in cell cycle regulation.
- βοΈ In normal cells, the RAS protein is inactive when bound to GDP and becomes active upon binding to GTP, a process facilitated by a GTP exchange factor.
- π The RAS protein activates transcription factors that promote cell cycle progression and division.
- π The GTPase activity, which involves a GTPase-activating protein (GAP), is crucial for inactivating RAS and controlling cell growth.
- 𧬠Mutations in the RAS protein's GTPase activity can lead to permanent activation and uncontrolled cell division.
- π For oncogenes, a single mutation can lead to cancer growth due to the gain of function, unlike tumor suppressor genes which require two 'hits'.
Q & A
What are the two main groups of genes involved in cancer development?
-The two main groups of genes involved in cancer development are tumor suppressor genes and proto-oncogenes.
How do proto-oncogenes contribute to cell growth and division?
-Proto-oncogenes produce proteins that encourage the cell to move through the cell cycle and divide. When they mutate, they become oncogenes that promote cell division and the development of cancer.
What is the difference between proto-oncogenes and oncogenes?
-Proto-oncogenes are the normal forms of genes that encourage cell division. Oncogenes are mutated forms of proto-oncogenes that are active all the time, promoting uncontrolled cell division.
How do oncogenes differ from tumor suppressor genes in terms of function?
-Tumor suppressor genes act like brakes to stop cells from moving through the cell cycle, while oncogenes act like accelerators, promoting cell growth and division.
Why is a gain of function in proto-oncogenes significant for cancer development?
-A gain of function in proto-oncogenes turns them into oncogenes, which can lead to uncontrolled cell division and cancer development because only one copy of the gene needs to mutate for this to occur.
What is the role of the RAS protein in normal cell function?
-In normal cells, the RAS protein is bound to GDP and must be activated by exchanging GDP for GTP, which is facilitated by a GTP exchange factor. This activation leads to the progression of the cell cycle and cell division.
How does the RAS protein become active, and what is its role in cell division?
-The RAS protein becomes active by substituting GDP for GTP, which is facilitated by a GTP exchange factor. Once active, it activates transcription factors that lead to the activation of genes involved in cell cycle progression and division.
What is the significance of the GTPase activity in the RAS protein?
-GTPase activity is significant because it deactivates the RAS protein by breaking down GTP to GDP, providing a way to control the RAS activity and thus controlling cell growth and division.
What happens if the GTPase activity portion of the RAS protein mutates?
-If the GTPase activity portion of the RAS protein mutates, it may not be able to break down GTP, leading to the RAS protein being permanently active and causing uncontrolled cell division.
How does the mutation of proto-oncogenes differ from that of tumor suppressor genes in terms of cancer development?
-For tumor suppressor genes, both copies need to be inactivated (two hits) to lead to cancer development, whereas for oncogenes, only one mutation is needed to promote cancer growth due to a gain of function.
Outlines
𧬠Understanding Proto-oncogenes and Oncogenes
This paragraph delves into the molecular basis of cancer, focusing on proto-oncogenes and oncogenes. It explains how mutations in DNA can lead to the production of faulty proteins, which in turn give cells cancerous characteristics known as the 'hallmarks of cancer.' Proto-oncogenes are genes that, in their normal state, encourage cell division. However, when mutated, they become oncogenes, promoting uncontrolled cell division and cancer development. The video uses the analogy of a car's accelerator to describe oncogenes, emphasizing that only one mutation is needed to activate the oncogene and lead to cancer. The Ras gene and its role in cell cycle regulation are also discussed, highlighting how mutations in the gene's GTPase activity can result in permanent activation and uncontrolled cell division.
π The Impact of Mutations on Tumor Suppressor Genes and Oncogenes
The second paragraph contrasts the effects of mutations on tumor suppressor genes and oncogenes. It explains that tumor suppressor genes act as 'brakes' on cell division, and both copies must be inactivated (a 'two-hit' scenario) for cancer to develop. In contrast, oncogenes act like an 'accelerator,' and only one mutation is required to promote cancer growth. This distinction is crucial for understanding how genetic mutations can lead to different outcomes in cancer development.
Mindmap
Keywords
π‘Proto-oncogenes
π‘Oncogenes
π‘Mutations
π‘Cell Cycle
π‘Tumor Suppressor Genes
π‘Hallmarks of Cancer
π‘GTP (Guanosine Triphosphate)
π‘GDP (Guanosine Diphosphate)
π‘GTPase Activity
π‘GTPase-Activating Protein (GAP)
π‘Gain of Function
Highlights
Cancer develops due to mutations in DNA that lead to the production of faulty proteins.
These proteins give cells certain characteristics known as the hallmarks of cancer.
Genes involved in cancer can be divided into tumor suppressor genes and proto-oncogenes.
Proto-oncogenes produce proteins that encourage cell division and movement through the cell cycle.
When proto-oncogenes mutate, they become oncogenes and promote cell division, leading to cancer.
Tumor suppressor genes act as brakes, while oncogenes act as accelerators in cell cycle control.
A gain in function of proto-oncogenes turning them into oncogenes leads to cancer growth.
For a gene to produce a properly functional protein, both copies must be taken out in the case of tumor suppressor genes.
Only one copy of an oncogene needs to mutate to promote cancer growth due to a gain in function.
The most commonly mutated oncogene in human cancers is the RAS gene.
The RAS protein is bound to GDP in its inactive state.
GTP exchange factors activate the RAS protein by substituting GDP with GTP.
Activated RAS protein leads to the activation of genes involved in cell cycle progression and division.
GTPase activity, with the help of GAP proteins, inactivates RAS by breaking down GTP to GDP.
Mutations in the GTPase activity portion of RAS can lead to permanent activation and uncontrolled cell division.
Tumor suppressor genes prevent cell growth and division, while oncogenes promote it.
Loss of function in tumor suppressor genes leads to cancer development, while a gain of function in oncogenes does.
Tumor suppressor genes require two hits (mutations in both copies), whereas oncogenes need only one mutation.
Transcripts
hello and welcome back to oncology for
medical students in this section of
videos on the molecular basis of cancer
this video will cover proto-oncogenes
and oncogenes in
the previous videos we talked about how
cancers develop as a result of mutations
to DNA how these changes lead to the
production of faulty proteins and how
these proteins give the cells certain
characteristics known as the hallmarks
of cancer we've also talked about how
the genes involved in these changes can
also be divided into two groups tumor
suppressor genes covered in the last
video and proto-oncogenes
cells contain many genes that produce
proteins that encourage the cell to move
through the cell cycle and divide the
normal forms of these genes are called
pro so oncogenes when they mutate way
that they are active all the time they
promote cell division on the development
of cancer the mutated forms of these
genes are called oncogenes
where tumor suppressor genes stop the
cells moving through the cell cycle like
the brakes of a car oncogenes are like
the accelerator pedal
where a loss of function of tumor
suppressor genes promote the growth of
cancer it's a gain in function of proton
code genes turning them into oncogenes
that Leeson leads to the growth of
cancers
because we have two copies of each gene
to stop a gene from producing a properly
functional protein both copies have to
be taken out this type of loss of
function applies to tumor suppressor
genes but this isn't the case with
oncogenes because we're talking about
genes that gainer function it's only
necessary for one copy to become mutated
to promote the growth of cancer
the most commonly mutated oncogene in
human cancers is the rats on coaching to
see how it functions again we'll have to
have a look inside the cell
in normal cells in its inactive state
the Rass protein is bound to a molecule
called gdp guanosine diphosphate in
order to become active the Rass gene
must substitute the gdp molecule for
another GTP guanosine triphosphate this
happens by the action of a protein
called a guanosine triphosphate or GTP
exchange factor this type of protein
exchanges the gdp on the inactive rass
protein for a gtp
which activates the wrasse protein
Russ then in turn activates a number of
transcription factors that lead to the
activation of genes involved in
progressing through the cell cycle and
dividing
you
the wrasse protein then deactivates by
the action of something called gtp A's
activity this means it breaks down the
gtp to GDP it does this with the help of
a protein called a GTP A's accelerating
protein or gap
the inactivation is very important it
provides a way of controlling the rats
activity and therefore controlling self
growth and division
if the portion of the wrasse protein
responsible for the gtp A's activity
mutates it may not be able to break down
the gtp this means that the gtp is stuck
bound to the wrasse protein and it's
permanently active leading to
uncontrolled cell division
because the mutation is leading to a
gain of function only one copy of the
gene needs to mutate to causes to happen
now that will cover both tumor
suppressor genes and oncogenes I thought
would finish with a quick comparison
where tumor suppressor genes are
involved in preventing cell growth and
division proto-oncogenes or the mutated
counterparts oncogenes promote cell
growth and division
it's normally a loss of function of
tumor suppressor genes that leads to the
development of cancers whereas on the
other hand with uncle genes it's a gain
of function
to use the car analogy the tumor
suppressor genes are like the car breaks
on the cell cycle and the onion the case
of oncogenes they like the car
accelerator
because we have two copies of each gene
and the case of tumor suppressor genes
you need both copies to be taken out to
lead to the development of cancer so
they need two hits and the case of
oncogenes they just need one mutation
thank you
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