Difference between revisions of "Team:SCUT-China B/Description"

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When cancer hits,what can we do？Cheothearapy？Radiation？Or surgery？All above is a choice，but seems to do really a lot of harm to our body，killing cancer cells as well as regular cells.
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  When cancer hits, what can we do？Chemotherapy？Radiation？Or surgery？All above is a choice，but seems to do really a lot of harm to our body，killing cancer cells as well as normal cells. So, it occurs to us, why not let the cancer cells to apoptosis themselves?  
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So,it occurs to us,why not let the cancer cells to apoptosis themselves?
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We learned that we can activate a certain gene or inhibit a certain gene, both are able to cause series of changes in cells, ending up in apoptosis.
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To activate apoptosis,we choose the mitochondria pathway.Let’s put it in a simple way:when there are more bax protein and less bcl-2 protein,the outer mitochondria membrane permeability will increase,releasing substance that will trigger caspase enzyme to cut the DNA,causing apoptosis.
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  What’s more, gene regulation therapy makes it easier for our therapy to “recognize” the cancer cells from normal cells. Just like a switch, the apoptosis system will only be activated when the plasmid recognize that this is a cancer cell. There are differences between cancer cells and normal cells and we take advantage of that, design our plasmid in a certain way ,making it able decide whether this is a cancer cell needed to go apoptosis or this is a normal cell and leave it alone.
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So how to regulate the genes?
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Well,here comes the crispr system. Using a sgRNA to guide cas9 protein to a certain sequence and the cas9 protein will act as a DNA cutting enzyme.
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So, inactive the cas9 protein and attach it to VP64——substance that will attract transcription factors and the sgRNA will guide our cas9 protein to certain sequence,activating the transcription of bax gene, and in the end, we got more bax protein.
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And, inactive the cas9 protein and let the sgRNA guide it to a certain sequence that will block the way of transcription enzyme so that bcl-2 gene will not be able to transcripted, ending up in less bcl-2 protein.
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Next, we want to add tumour specific transcription promotor so that our crispr activate apoptosis sysmtem will only be triggered in tumout cells, protecting the normal cells.
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Revision as of 14:24, 15 July 2016

 When cancer hits, what can we do？Chemotherapy？Radiation？Or surgery？All above is a choice，but seems to do really a lot of harm to our body，killing cancer cells as well as normal cells. So, it occurs to us, why not let the cancer cells to apoptosis themselves?

We learned that we can activate a certain gene or inhibit a certain gene, both are able to cause series of changes in cells, ending up in apoptosis. 

 What’s more, gene regulation therapy makes it easier for our therapy to “recognize” the cancer cells from normal cells. Just like a switch, the apoptosis system will only be activated when the plasmid recognize that this is a cancer cell. There are differences between cancer cells and normal cells and we take advantage of that, design our plasmid in a certain way ,making it able decide whether this is a cancer cell needed to go apoptosis or this is a normal cell and leave it alone.