ArticleJBMR plus2025
KRAS regulates IL-17 signal activity by affect the metastasis of osteosarcoma via an IL-17A-dependent manner.
Article in JBMR plus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Corrections and comments
- Erratum issued
Authors and funding
7 authors.
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Abstract
Dysregulation of Kirsten rat sarcoma virus (KRAS) plays crucial roles in many tumors. It is reported that KRAS could promote proliferation of osteosarcoma (OS) cells. Nonetheless, the contribution of KRAS to the invasion and spread of OS is still not well understood. This study aimed to investigate KRAS-driven metastasis and the mechanisms behind it in human OS. Tissue microarrays were utilized to assess KRAS expression and its relationship with clinicopathological characteristics. The migratory and invasive abilities of OS cells were evaluated through wound-healing assays and transwell analysis. Furthermore, the regulatory mechanisms of KRAS in human OS were analyzed using RNA sequencing, tandem mass tags assays, multiple immunofluorescence assays, micro-CT, and bioluminescence imaging. In vivo experiments were conducted using established lung metastatic models. Our data showed that downregulation of KRAS in human OS cells could inhibit cell migration and invasion in vitro and in vivo (tumor metastasis model by tail vein injection in BALB/c nude mice). We identify IL-17A, a crucial marker of IL-17 signal pathway, as a downstream target of KRAS. The reduction of KRAS may suppress matrix metalloproteinase (MMP1), MMP3, and MMP9, which are recognized as proteins associated with tumor metastasis, through a mechanism dependent on IL-17 signaling. In summary, these findings indicate that KRAS could serve as a potential biomarker for therapeutic strategies in human OS. Mechanistically, our data revealed that KRAS knockdown affects tumor metastasis by inactivating IL-17 signal pathway via IL-17A-dependent manner.
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