{
  "abstract": "Background Ferroptosis, a newly identified form of cell death, plays a significant role in colorectal cancer (CRC) progression; however, its specific regulatory mechanisms remain incompletely understood.Methods We investigated TRIM69 expression and its prognostic significance in clinical CRC specimens using the TCGA database and tissue samples. Subsequently, in vitro studies explored TRIM69’s role in ferroptosis through overexpression or knockdown of the TRIM69 gene. Glutathione and ferrous ion levels were measured using kits. RT-qPCR was employed to detect mRNA expression levels of key ferroptosis molecules. Western blotting analyzed downstream molecules and pathways regulated by TRIM69. An in vivo xenograft model was established to validate TRIM69’s role in ferroptosis.Results This study utilized the TCGA database and clinical tissue samples to analyze TRIM69 expression and its prognostic value in CRC. Results demonstrated that low TRIM69 expression in CRC tissues was significantly associated with poor patient prognosis ( IDDF2026-ABS-0282 Figure 1. TRIM69 expression is decreased in CRC tissues and is negatively associated with poor prognosis). In vitro functional experiments involving TRIM69 overexpression or knockdown, combined with glutathione and ferrous ion level assays and RT-qPCR analysis, confirmed that TRIM69 significantly inhibits CRC cell proliferation and induces ferroptosis (IDDF2026-ABS-0282 Figure 2. Overexpression of TRIM69 inhibits the proliferation of CRC cells and promotes their ferroptosis, IDDF2026-ABS-0282 Figure 3. Knocking down TRIM69 promotes the proliferation of CRC cells and inhibits ferroptosis). RNA sequencing, Western blotting, and co-immunoprecipitation (CO-IP) experiments further (IDDF2026-ABS-0282 Figure 4. TRIM69 regulates the MAPK pathway via ASK1). Inhibition of this pathway reverses the altered cell proliferation and ferroptosis phenotypes induced by TRIM69 knockdown (IDDF2026-ABS-0282 Figure 5. TRIM69 inhibits cell proliferation and promotes ferroptosis in CRC cells by regulating the ASK1/MAPK signaling pathway). Furthermore, an in vivo xenograft model validated that TRIM69 promotes ferroptosis and inhibits tumor growth (IDDF2026-ABS-0282 Figure 6. Overexpression of TRIM69 inhibits in vivo growth of CRC).Conclusions These findings indicate that TRIM69 enhances CRC ferroptosis by regulating the ASK1/MAPK pathway, thereby suppressing tumor proliferation. This suggests that targeting the TRIM69-ASK1/MAPK axis may offer a novel therapeutic strategy for CRC treatment.Abstract IDDF2026-ABS-0282 Figure 1Abstract IDDF2026-ABS-0282 Figure 2Abstract IDDF2026-ABS-0282 Figure 3Abstract IDDF2026-ABS-0282 Figure 4Abstract IDDF2026-ABS-0282 Figure 5Abstract IDDF2026-ABS-0282 Figure 6",
  "authors": [
    {
      "affiliations": [
        "Department of Gastroenterology, The First Affiliated Hospital of Soochow University, China"
      ],
      "name": "Nan Gao"
    },
    {
      "affiliations": [
        "Department of Gastroenterology, The First Affiliated Hospital of Soochow University, China"
      ],
      "name": "Zhijie Zheng"
    },
    {
      "affiliations": [
        "Department of Gastroenterology, The First Affiliated Hospital of Soochow University, China"
      ],
      "name": "Rui Li"
    },
    {
      "affiliations": [
        "Department of Gastroenterology, The First Affiliated Hospital of Soochow University, China"
      ],
      "name": "Weichang Chen"
    }
  ],
  "title": "IDDF2026-ABS-0282 TRIM69 inhibits cell proliferation and promotes ferroptosis in colorectal cancer via the ASK1/MAPK axis",
  "uid": "2f605ea4-9ba3-589b-884f-cbbf80041542"
}