Publication: AB064. TRIM29: a novel gene involved in DNA repair mechanisms
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Issued Date
2017
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eng
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Mahidol University
Rights Holder(s)
Society for Translational Medicine (STM)
Bibliographic Citation
Annals of Translational Medicine. Vol 5, Suppl. 2 (Sep 2017)
Suggested Citation
Rakkreat Wikiniyadhanee, Tassanee Lerksuthirat, Wasana Stitchantrakul, Sermsiri Chitphuk, Donniphat Dejsuphong AB064. TRIM29: a novel gene involved in DNA repair mechanisms. Annals of Translational Medicine. Vol 5, Suppl. 2 (Sep 2017). Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/61244
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Title
AB064. TRIM29: a novel gene involved in DNA repair mechanisms
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Abstract
Background: Cytotoxic chemotherapy and/or radiation therapy inducing DNA damage is a part of cancer treatment. Tripartite motif 29 (TRIM29) is highly expressed in many malignancies; for example, pancreatic cancer which is notorious resistant to cytotoxic chemotherapy and radiation therapy. TRIM29 is a member of the TRIM protein family composed of more than 70 members associated with a broad of biological processes. Originally, TRIM29 gene was described as a candidate gene responsible for ataxia- telangiectasia (AT); however, TRIM29 was dismissed as AT-causing gene after ataxia- telangiectasia mutated (ATM) was discovered as a causative gene for AT. A few studies about TRIM29 suggested that it was involved in DNA damage response and high expression of TRIM29 promoted resistance to ionizing radiation (IR), which induces DNA double strand breaks (DSB). Nevertheless, the functions of TRIM29 in DNA damage responses and/or DNA repair mechanisms are still unclear.
Methods: To investigate the functions of TRIM29 in DNA repair mechanisms, wild-type DT40 (WT) and mutant strains have been selected and used as a model. Firstly, the researchers generated the TRIM29 knockout (TRIM29-/-/-/+).
Results: The growth analysis showed that TRIM29-/-/-/+ was comparable to WT. The results of DNA-damaging agent sensitivity using clonogenic survival assays indicated that TRIM29-/-/-/+ clones displayed increased sensitivity to topoisomerase 2 inhibitors which induce DNA DSBs repaired by non-homologous end joining (NHEJ) pathway. The TRIM29-/-/-/+ clones also exhibited mild sensitivity to camptothecin and cisplatin, indicating that TRIM29 plays a role in DNA DSB repair mechanisms.
Conclusions: Further study of TRIM29 in response to DNA DSBs may help improve the understanding of functions of TRIM29. In the future, TRIM29 might be a target for anti-cancer drug, leading to improvement of cancer treatment effectiveness.