PharmaMar has presented the novel data on how plitidepsin inhibits the growth of the tumor cells at the AACR meeting (American Association for Cancer Research) in Chicago.
Under the title "eEF1A2 interacts with and inhibits PKR to enhance cancer cell survival", the Company has presented the newly discovered oncogenic properties of eEF1A2, the target of plitidepsin. PharmaMar has discovered that this protein bond to the enzyme favoring in this way tumor growth. Plitidepsin inhibits this interaction obtaining the induction of cell death.
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‘Bonding of plitidepsin to eEF1A2 protein limits the tumor growth.’
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Indeed, this is one step more in the understanding of the mechanism of action of plitidepsin. Up to today, PharmaMar has described that the target of plitidepsin is the eEF1A2 protein, over expressed in tumor cells, as in breast cancer or multiple myeloma. Through its bonding to eEF1A2, plitidepsin annuls the oncogenic properties of its target.
For example, the bonding between eEF1A2 and Peroxiredoxin-1 controls the oxidative stress levels that favor tumor cell survival. Plitidepsin, on interrupting eEF1A2's bonding with Peroxiredoxin-1, increases the oxidative stress levels, provoking tumor cell death.
![New Insights on Dependency Factors of Breast Cancer Cells found]( "New Insights on Dependency Factors of Breast Cancer Cells found")
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In the same way, plitidepsin interrupts the bonding of eEF1A2 with sphingosine kinase in the same way, an enzyme that regulates the level of the metabolites responsible for cell proliferation. The bonding of Plitidepsin to eEF1A2 inhibits the formation of the above mentioned metabolites, thus also limiting tumor growth.
In all cases, the final consequence of these interactions of plitidepsin with eEF1A2 is the activation of a suicidal program of cells called apoptosis.
Source: Eurekalert
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PIK3CA, a gene that drives cancer can control methionine dependency of breast cancer cells. This could be a novel approach to treating a variety of breast tumors.
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In the same way, plitidepsin interrupts the bonding of eEF1A2 with sphingosine kinase in the same way, an enzyme that regulates the level of the metabolites responsible for cell proliferation. The bonding of Plitidepsin to eEF1A2 inhibits the formation of the above mentioned metabolites, thus also limiting tumor growth.
In all cases, the final consequence of these interactions of plitidepsin with eEF1A2 is the activation of a suicidal program of cells called apoptosis.
Source: Eurekalert
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