ArticleCancer gene therapy2022
GLIPR1 promotes proliferation, metastasis and 5-fluorouracil resistance in hepatocellular carcinoma by activating the PI3K/PDK1/ROCK1 pathway.
Article in Cancer gene therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Multi-omics and mendelian randomization uncover microbial-metabolite-gene interactions in age-related hearing loss.AMB Express · 2026Article
- Identification of circulating miRNA alterations in diabetes patients excluding periodontitis effects: insights into target gene downregulation in diabetic complications.Annals of medicine · 2025Article
- Macrophage marker gene-driven prognostic models for esophageal cancer: integrating multi-omics analysis and therapeutic strategies.3 Biotech · 2025Article
- Mechanisms of drug resistance in hepatocellular carcinoma.Biological procedures online · 2025Review
- CRISPR/Cas9 Screening Highlights PFKFB3 Gene as a Major Contributor to 5-Fluorouracil Resistance in Esophageal Cancer.Cancers · 2025Article
- CAP superfamily proteins in human: a new target for cancer therapy.Medical oncology (Northwood, London, England) · 2024Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatocellular carcinoma (HCC) contributes to a heavy disease burden for its high prevalence and poor prognosis, with limited effective systemic therapies available. In the era of precision medicine, treatment efficacy might be improved by combining personalized systemic therapies. Since oncogenic activation is one of the primary driving forces in HCC, characterization of these oncogenes can provide insights for developing new targeted therapies. Based on RNA sequencing of epithelial-mesenchymal transition (EMT)-induced HCC cells, this study discovers and characterizes glioma pathogenesis-related protein 1 (GLIPR1) that robustly drives HCC progression and can potentially serve as a prognostic biomarker and therapeutic target with clinical utility. GLIPR1 serves opposing roles and involves distinct mechanisms in different cancers. However, based on integrated in-silico analysis, in vitro and in vivo functional investigations, we demonstrate that GLIPR1 plays a multi-faceted oncogenic role in HCC development via enhancing tumor proliferation, metastasis, and 5FU resistance. We also found that GLIPR1 induces EMT and is actively involved in the PI3K/PDK1/ROCK1 singling axis to exert its oncogenic effects. Thus, pre-clinical evaluation of GLIPR1 and its downstream factors in HCC patients might facilitate further discovery of therapeutic targets, as well as improve HCC chemotherapeutic outcomes and prognosis.
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.