ArticleCell death & disease2014
GLI2 induces genomic instability in human keratinocytes by inhibiting apoptosis.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
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- Antitumor activity and mechanism of cucurbitacin B in A549/DDP cells.Naunyn-Schmiedeberg's archives of pharmacology · 2023Article
- Hedgehog signaling and the glioma-associated oncogene in cancer radioresistance.Frontiers in cell and developmental biology · 2023Review
- GLI1: A Therapeutic Target for Cancer.Frontiers in oncology · 2021Review
- Hedgehog Signal Inhibitor GANT61 Inhibits the Malignant Behavior of Undifferentiated Hepatocellular Carcinoma Cells by Targeting Non-Canonical GLI Signaling.International journal of molecular sciences · 2020Article
- Expression profiles of p53/p73, NME and GLI families in metastatic melanoma tissue and cell lines.Scientific reports · 2019Article
- Insight into the Etiology of Undifferentiated Soft Tissue Sarcomas from a Novel Mouse Model.Molecular cancer research : MCR · 2019Article
- Non-canonical Hedgehog Signaling Pathway in Cancer: Activation of GLI Transcription Factors Beyond Smoothened.Frontiers in genetics · 2019Review
- Temporal DNA-PK activation drives genomic instability and therapy resistance in glioma stem cells.JCI insight · 2018Article
- Hedgehog signaling: modulation of cancer properies and tumor mircroenvironment.Molecular cancer · 2016Review
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- Inhibition of ERK1/2 down-regulates the Hippo/YAP signaling pathway in human NSCLC cells.Oncotarget · 2015Article
- A novel multiplexed, image-based approach to detect phenotypes that underlie chromosome instability in human cells.PloS one · 2015Article
- BCC or not: Sufu keeps it in check.Oncoscience · 2015Article
- Azelaic acid stimulates catalase activation and promotes hair growth through upregulation ofAvicenna journal of phytomedicineArticle
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal Sonic Hedgehog signalling leads to increased transcriptional activation of its downstream effector, glioma 2 (GLI2), which is implicated in the pathogenesis of a variety of human cancers. However, the mechanisms underlying the tumorigenic role of GLI2 remain elusive. We demonstrate that overexpression of GLI2-β isoform, which lacks the N-terminal repressor domain (GLI2ΔN) in human keratinocytes is sufficient to induce numerical and structural chromosomal aberrations, including tetraploidy/aneuploidy and chromosomal translocations. This is coupled with suppression of cell cycle regulators p21(WAF1/CIP1) and 14-3-3σ, and strong induction of anti-apoptotic signalling, resulting in a reduction in the ability to eliminate genomically abnormal cells. Overexpression of GLI2ΔN also rendered human keratinocytes resistant to UVB-mediated apoptosis, whereas inhibition of B-cell lymphoma 2 (BCL-2) restored endogenous (genomic instability (GIN)) and exogenous (UVB) DNA damage-induced apoptosis. Thus, we propose that ectopic expression of GLI2 profoundly affects the genomic integrity of human epithelial cells and contributes to the survival of progenies with genomic alterations by deregulating cell cycle proteins and disabling the apoptotic mechanisms responsible for their elimination. This study reveals a novel role for GLI2 in promoting GIN, a hallmark of human tumors, and identifies potential mechanisms that may provide new opportunities for the design of novel forms of cancer therapeutic strategies.
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