ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Ubiquitination-Dependent LLGL2 Degradation Drives Colorectal Cancer Progression via THBS3 mRNA Stabilization.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Ubiquitination-Dependent LLGL2 Degradation Drives Colorectal Cancer Progression via THBS3 mRNA Stabilization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Super-Enhancer DrivesAnimals : an open access journal from MDPI · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Colorectal cancer (CRC) is the second most common cause of cancer-related deaths worldwide is highly associated with distant organ metastasis. Lethal(2) giant larvae protein homolog 2 (LLGL2) is often dysregulated in various tumors; however, the pathogenesis of CRC remains unclean. This study highlighted the tumor suppressor function of LLGL2 in CRC. Depleted LLGL2 exhibits the pro-CRC effects. RNA sequencing reveals that LLGL2 suppresses CRC progression by inhibiting the phosphoinositide 3-kinase (PI3K)-protein kinase B (PKB)/Akt pathway. Further analysis using RNA immunoprecipitation sequencing and shotgun mass spectrometry indicated that LLGL2 primarily regulates the stability of thrombospondin 3 (THBS3) mRNA by interacting with CCR4-NOT transcription complex subunit 1 (CNOT1), thus inactivating the PI3K-Akt pathway. Additionally, MDM2 acts as an upstream modulator of LLGL2 and promotes its degradation via the proteasomal pathway. This novel mechanism reveals potential therapeutic targets for CRC treatment and enhanced the understanding of how CRC progression can be controlled.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.