Scientists have investigated the use of certain proteins to make cancer treatments more effective with the use of
analytical chemistry methods.
In a study published by the Molecular Cancer journal, the team of scientists aimed to provide clarity to the mechanism underlying the effects of DNA-dependent protein kinase (DNA-PK) on cisplatin sensitivity.
DNA-PK is known to bind to DNA double strand breaks (DSBs) and initiates the ends joining, restraining DNA-PK therefore makes cancer cells more sensitive to being killed off by cisplatin in chemotherapy procedures.
However, little is known as to how or why silencing the expression of the catalytic subunit of DNA-PK has this effect.
Using analytical chemistry processes including tandem mass spectrometry revealed that DNA-PK and the facilitator of chromatin transcription (FACT) both play roles in DNA repair.
As DNA-PK regulates the process of cell death, restraining it can allow chemotherapy treatments be become more effective, however, silencing FACT allows both apoptosis and necrosis.
To this end, targeting DNA repair in cancer patients may have different therapeutic effects, depending upon the roles played by factors targeted.
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