AI Article Synopsis
- Colorectal cancer (CRC) is a serious disease with high fatality rates, and the tumor suppressor TSPYL2's role in CRC is not well understood.
- Research found that in drug-resistant CRC tissues, TSPYL2 is downregulated while SIRT1 is upregulated, leading to enhanced resistance to the drug gefitinib (GEF).
- TSPYL2 appears to reduce GEF resistance and DNA damage repair in CRC by inhibiting SIRT1's effect on FOXO3, suggesting that TSPYL2 could be a potential target for CRC therapy.
Article Abstract
Colorectal cancer (CRC) is a malignancy with high mortality. TSPYL2 participates in tumor suppression but its role in CRC remains unknown. TSPYL2 was downregulated and SIRT1 was upregulated in gefitinib drug-resistant (GEF-DR) tissues of patients with CRC. The GEF-resistant cells, HCT116 and HCT-15, were successfully established. The knockdown of TSPYL2 promoted resistance to GEF in CRC cells. Interestingly, immunofluorescence and western blot assays demonstrated that TSPYL2 inhibited DNA damage repair in HCT-15 and HCT116 GEF-resistant cells. Mechanically, TSPYL2 reduced the resistance to GEF and inhibited DNA damage repair via suppressing SIRT1-mediated FOXO3 deacetylation. TSPYL2 consistently inhibited tumor growth and decreased resistance to GEF . TSPYL2 reduced resistance to GEF and suppressed DNA damage through downregulating SIRT1-mediated FOXO3 deacetylation, indicating that TSPYL2 might be a novel therapeutic target in CRC.
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| http://dx.doi.org/10.4155/fmc-2021-0136 | DOI Listing |
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