ArticleInternational journal of molecular sciences2026
Loss of LLGL1 Elevates EGFR/RAS/MAPK Signaling and Remodels EMT Markers in Huh-7 Hepatocellular Carcinoma Cells.
Article in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- NHSL3 knockout modulates sorafenib response, growth, and motility in hepatocellular carcinoma cell models.Molecular biology reports · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
Loss of epithelial polarity is a critical driver of tumor progression; however, how core polarity regulators interface with oncogenic signaling pathways in hepatocellular carcinoma (HCC) remains incompletely defined. LLGL scribble cell polarity complex component 1 (LLGL1) is an evolutionarily conserved polarity protein with well-established tumor-suppressive roles in multiple epithelial malignancies. Nevertheless, how LLGL1 loss shapes oncogenic signaling outputs and cellular phenotypes in HCC remains unclear. In this study, we investigated the consequences of LLGL1 knockout (KO) in epithelial-like Huh-7 HCC cells. LLGL1 loss resulted in enhanced proliferative capacity and increased clonogenic potential, accompanied by altered cell-cycle distribution characterized by reduced G1-phase and increased S-phase fractions (
Indexed as
Identifiers
What Socratic 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 Socratic graph.