AI Article Synopsis
- TMZ is a common chemotherapy drug for colorectal cancer, but its effectiveness is reduced due to cancer cell resistance linked to the base excision repair (BER) pathway.
- By inhibiting the Polβ-dependent BER pathway, the therapeutic impact of TMZ can be significantly enhanced.
- The study identified a new Polβ inhibitor, 10 D, using phage display technology, which increases CRC cells' sensitivity to TMZ, potentially improving chemotherapy outcomes.
Article Abstract
The therapeutic efficacy of TMZ, a common used drug for chemotherapy, is limited by the resistance from colorectal cancer cells. Base excision repair (BER) pathway has been identified as one of the reasons for drug resistance. By blocking Polβ-dependent BER (Base Excision Repair) pathway, the efficacy of TMZ treatment can be improved greatly. Several Polβ inhibitors that have been identified could not become approved drugs due to lack of potency or specificity. To find therapeutic candidates with exquisite specificity and high affinity to Polβ, phage display technology was used in the current research. We screened out a candidate Polβ inhibitor, 10 D, that can inhibit the activity of Polβand SP-BER (Short-Patch Base excision Repair) pathway. Co-treatment with 10 D enhanced the sensitivity of colorectal cancer (CRC) cells to TMZ both and . Our data suggested that the novel Polβ inhibitor we identified can improve TMZ efficacy and optimize CRC chemotherapy.
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| http://dx.doi.org/10.1080/1120009X.2021.2009987 | DOI Listing |
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