ArticleAmerican journal of cancer research2026
CAAP1 suppresses tumor growth and metastasis via interacting with EIF3I in high-grade serous ovarian carcinoma.
Article in American journal of cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
High-grade serous ovarian cancer (HGSOC) is frequently diagnosed at advanced stages with refractory peritoneal metastases, resulting in a dismal prognosis. Caspase activity and apoptosis inhibitor 1 (CAAP1), an apoptosis regulator with debated functions, has an unexplored role in HGSOC progression. Herein, the prognostic value of CAAP1 was evaluated using The Cancer Genome Atlas (TCGA) database and clinical tissue samples. The effects of CAAP1 on HGSOC cell proliferation, migration, and apoptosis resistance were examined via cell counting kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (EdU) incorporation, wound healing, Transwell, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays. A subcutaneous xenograft model was employed to verify the tumor-suppressive role of CAAP1 in vivo. Furthermore, liquid chromatography-tandem mass spectrometry (LC-MS/MS) and co-immunoprecipitation (Co-IP) were performed to identify and validate CAAP1-interacting proteins, with Western blotting utilized to assess downstream signaling alterations. Our results demonstrated that CAAP1 downregulation was significantly correlated with poor prognosis in HGSOC patients. Functionally, CAAP1 knockdown promoted HGSOC cell proliferation, migration, and apoptosis resistance, whereas CAAP1 overexpression exerted opposite inhibitory effects. In vivo experiments corroborated that CAAP1 overexpression effectively suppressed tumor growth. Mechanistically, CAAP1 was found to interact with eukaryotic translation initiation factor 3 subunit I (EIF3I) to modulate the expression of cancer-related proteins. Collectively, this study establishes that CAAP1 functions as a tumor suppressor in HGSOC by binding to EIF3I, thereby restraining tumor growth and metastasis.
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