ReviewSeminars in cell & developmental biology2014
Context-dependent signal integration by the GLI code: the oncogenic load, pathways, modifiers and implications for cancer therapy.
Review in Seminars in cell & developmental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 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
92 citing papers in PubMed, 150 citations in OpenAlex.
- The SHH/GLI target Netrin-1 supports self-renewal in medulloblastoma tumor cells.Cell communication and signaling : CCS · 2026Article
- GLI3 in cancer: a context-dependent regulator with diagnostic, prognostic, and therapeutic potential.Frontiers in immunology · 2026Review
- The Drosophila epidermal growth factor receptor pathway regulates Hedgehog signalling and cytoneme behaviour.Nature communications · 2025Article
- Article
- Article
- GANT-61 induces cell cycle resting and autophagy by down-regulating RNAP III signal pathway and tRNA-Gly-CCC synthesis to combate chondrosarcoma.Cell death & disease · 2023Article
- Network motifs and hypermotifs in TGFβ-induced epithelial to mesenchymal transition and metastasis.Frontiers in systems biology · 2023Article
- ERK2 MAP kinase regulates SUFU binding by multisite phosphorylation of GLI1.Life science alliance · 2022Article
- Advances in glioma-associated oncogene (GLI) inhibitors for cancer therapy.Investigational new drugs · 2022Review
- GLIS1 in Cancer-Associated Fibroblasts Regulates the Migration and Invasion of Ovarian Cancer Cells.International journal of molecular sciences · 2022Article
- Hedgehog/GLI signaling in hematopoietic development and acute myeloid leukemia-From bench to bedside.Frontiers in cell and developmental biology · 2022Review
- The Hedgehog Signaling Pathway in Idiopathic Pulmonary Fibrosis: Resurrection Time.International journal of molecular sciences · 2021Review
- Circular RNAs in Hedgehog Signaling Activation and Hedgehog-Mediated Medulloblastoma Tumors.Cancers · 2021Article
- Hedgehog Signaling in Myeloid Malignancies.Cancers · 2021Review
- Article
- Acute Myeloid Leukemia Mutations and Future Mechanistic Target to Overcome Resistance.Current treatment options in oncology · 2021Review
- Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021Review
- Hedgehog Signaling in Colorectal Cancer: All in the Stroma?International journal of molecular sciences · 2021Review
- Repurposing of posaconazole as a hedgehog/SMO signaling inhibitor for embryonal rhabdomyosarcoma therapy.American journal of cancer research · 2021Article
- Minibrain-related kinase/dual-specificity tyrosine-regulated kinase 1B implication in stem/cancer stem cells biology.World journal of stem cells · 2020Review
32 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Canonical Hedgehog (HH) signaling leads to the regulation of the GLI code: the sum of all positive and negative functions of all GLI proteins. In humans, the three GLI factors encode context-dependent activities with GLI1 being mostly an activator and GLI3 often a repressor. Modulation of GLI activity occurs at multiple levels, including by co-factors and by direct modification of GLI structure. Surprisingly, the GLI proteins, and thus the GLI code, is also regulated by multiple inputs beyond HH signaling. In normal development and homeostasis these include a multitude of signaling pathways that regulate proto-oncogenes, which boost positive GLI function, as well as tumor suppressors, which restrict positive GLI activity. In cancer, the acquisition of oncogenic mutations and the loss of tumor suppressors - the oncogenic load - regulates the GLI code toward progressively more activating states. The fine and reversible balance of GLI activating GLI(A) and GLI repressing GLI(R) states is lost in cancer. Here, the acquisition of GLI(A) levels above a given threshold is predicted to lead to advanced malignant stages. In this review we highlight the concepts of the GLI code, the oncogenic load, the context-dependency of GLI action, and different modes of signaling integration such as that of HH and EGF. Targeting the GLI code directly or indirectly promises therapeutic benefits beyond the direct blockade of individual pathways.
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.