Pdcd4-Rictor interaction suppresses mTORC2-PFKFB3 axis and tumorigenesis in NSCLC.
What this study shows
Pdcd4 binds Rictor via residues R105/K108/R110 to disrupt mTORC2 assembly and kinase activity, lowering PFKFB3 levels and suppressing glycolysis and NSCLC tumour growth.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: NSCLC cell lines; mouse xenograft; human tumour tissue) 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 | NSCLC cell lines; mouse xenograft; human tumour tissue |
| Journal | Neoplasia |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1016/j.neo.2026.101354 · PMID 42648032 · Free full text (PMC13544097) |
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 | Pdcd4 overexpression / knockdown; Rictor-binding-deficient mutants |
| Target | Rictor; mTORC2; PFKFB3 |
| Model | Human cell lines; mouse xenograft |
| Effect | Disrupted mTORC2 assembly and kinase activity, degraded PFKFB3, suppressed glycolysis and tumour growth |
In the Atlas
Related topics
Links in the pathway map
- Supports PDCD4 inhibits mTORC2
More studies on this topic
- S6K1- and betaTRCP-mediated degradation of PDCD4 promotes protein translation and cell growth (2006)
- Transient APC/C inactivation by mTOR boosts glycolysis during cell cycle entry (2025)
- TET1-mediated DNA demethylation and transcription activation of MRPS17 induces lung adenocarcinoma through PI3K-AKT-mTOR pathway. (2026)
- The kinase mTOR regulates the differentiation of helper T cells through the selective activation of signaling by mTORC1 and mTORC2 (2011)
Was this page useful?
Thank you. Your answer was counted anonymously.