The protein isoform produced in normal cells is known as PK-M1, while the one produced by cancer cells is known as PK-M2.
Online PR News – 22-April-2013 – California – 18th April 2013(http://www.realpharmacyrx.co/) : Cancer cells divide in an uncontrolled way. That's an essential feature of what makes them cancer cells when compared with normal cells. They've stopped through all the cell-cycle checkpoints and are continuously growing and dividing. To do this they need to increase their metabolism rate.
Therefore we can target the metabolic process of cancer cells and can specifically kill them.
While metabolic changes are an important feature in the alteration of normal cells into cancer cells they are not now thought to be cancer's primary cause. However, metabolic changes remain an attractive target for cancer therapy. One difference between metabolism in cancer and normal cells is the the production of a different version, or isoform, of a protein produced from the pyruvate kinase-M (PK-M) gene. The protein isoform produced in normal cells is known as PK-M1, while the one produced by cancer cells is known as PK-M2.
PK-M2 is highly expressed in cancer cells. It helps the cancer cell to consume far more glucose than normal, while using little of it for energy. Instead, the rest is used to make more substance with which to build more cancer cells.
PK-M1 and PK-M2 are produced in a mutually exclusive manner from the same gene, by a mechanism known as alternative splicing. When a gene's DNA is being copied into the mRNA, the intermediate template for making proteins, called the spliceosome cuts and pastes different pieces out of and into that mRNA molecule. The parts that are edited out are known as introns, while the final protein-coding mRNA consists of a parts pasted together known as exons. The part that fits into the PK-M1 gene-coding sequence is known as exon 9, while one which is replaced in PK-M2 is exon 10. In this way alternative splicing provides the cell with the ability to make many proteins from a single gene.
Expression of PK-M2 is favored in cancer cells by these proteins, which act to stop splicing for the PK-M1 isoform. Therefore target the splicing of PK-M using a technology called antisense is our goal.
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Balfour Morris is a Medical Student and a freelancer who is specialized in writing. He is associate with many Pharmacies for whom he writes news based on generic drugs and general health related issues.