ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
KIAA1429 Silencing ameliorates osteosarcoma progression through promoting ferroptosis via Nrf2/NQO1 axis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Decoding osteosarcoma pathogenesis: the pivotal influence of mEpigenetics · 2026Review
- KIAA1429 knockdown alleviates osteosarcoma progression by destabilizing SLC7A11 mRNA via m6A methylation to promote ferroptosis.International journal of oncology · 2026Article
- KIAA1429 as a therapeutic target in osteosarcoma: challenging the linear ferroptosis pathway and evaluating translational hurdles.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
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4 authors.
Funding
Abstract
backgroundOsteosarcoma (OS) is the most common primary malignant bone tumor. Recent insights into ferroptosis have opened new avenues for OS therapy. However, the role of KIAA1429 in regulating ferroptosis and its underlying mechanisms in OS remain unclear.
methodsThe effects of KIAA1429 silencing on ferroptosis were evaluated in OS cells treated with erastin alone or in combination with ferrostatin-1 (Fer-1), as well as in an OS mouse model administered sulfasalazine (SAS). Methylation sites on the Nrf2 and NQO1 transcripts were predicted using the SRAMP database and subsequently validated by MeRIP-qPCR. Furthermore, RTA-408 was employed to further investigate the impact of KIAA1429 knockdown on the Nrf2/NQO1 signaling pathway in OS cells.
resultsKIAA1429 silencing reduced cell viability and increased the expression of ferroptosis-related markers in erastin-treated OS cells, and these effects were reversed by Fer-1. Knockdown of KIAA1429 further enhanced SAS-induced ferroptosis and suppression of xenograft tumor growth. MeRIP-qPCR and dual-luciferase reporter assays demonstrated that KIAA1429 directly regulated Nrf2 via m6A-dependent modification of its 3'UTR. KIAA1429 depletion inhibited viability, migration, and invasion and promoted apoptosis of MG-63 and U2OS cells through suppression of the Nrf2/NQO1 signaling.
conclusionKIAA1429 silencing facilitates ferroptosis, thereby delaying OS progression, potentially through modulation of the Nrf2/NQO1 signaling pathway.
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