IGF2BP3-Mediated m6A Modification of OLR1 mRNA Promotes Immune Evasion in CRC via the PI3K/AKT/mTOR Pathway
What this study shows
IGF2BP3 stabilizes OLR1 via m6A RNA modification, activating PI3K/AKT/mTOR signaling which suppresses CD8+ T cell anti-tumor activity and drives immune evasion in colorectal cancer.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: CRC cell lines (human); TCGA dataset) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | CRC cell lines (human); TCGA dataset |
| Journal | Journal of Immunotherapy |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1097/CJI.0000000000000613 · PMID 42592954 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | OLR1 knockdown; IGF2BP3 modulation |
| Target | PI3K/AKT/mTOR pathway; OLR1; IGF2BP3; m6A RNA modification |
| Model | Human |
| Effect | m6A-stabilized OLR1 activates PI3K/AKT/mTOR to suppress CD8+ T cell function and enable CRC immune evasion; OLR1 knockdown restores T cell anti-tumor activity |
In the Atlas
Related topics
More studies on this topic
- Leniolisib and rapamycin in Activated PI3-Kinase-δ-syndrome: a retrospective ESID registry-based analysis (2026)
- The phosphoinositide 3-kinase pathway (2002)
- A dynamic network model of mTOR signaling reveals TSC-independent mTORC2 regulation (2012)
- Evidence for direct activation of mTORC2 kinase activity by phosphatidylinositol 3,4,5-trisphosphate (2011)
Was this page useful?
Thank you. Your answer was counted anonymously.