ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
Hedgehog/Gli1 signal pathway facilitates proliferation, invasion, and migration of cutaneous SCC through regulating VEGF.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Gli1 promotes the phenotypic transformation of valve interstitial cells through Hedgehog pathway activation exacerbating calcific aortic valve disease.International journal of biological sciences · 2023Article
- Associations of keratinocyte cancers with snp variants in the sonic hedgehog pathway.BMC cancer · 2022Article
- Suppressor of Fused Inhibits Skin Wound Healing.Advances in wound care · 2020Article
- Sonic Hedgehog/Gli1 Signaling Pathway Regulates Cell Migration and Invasion via Induction of Epithelial-to-mesenchymal Transition in Gastric Cancer.Journal of Cancer · 2020Article
- Krüppel-like factor 2 inhibits hepatocarcinogenesis through negative regulation of the Hedgehog pathway.Cancer science · 2019Article
- Regulation and Role of GLI1 in Cutaneous Squamous Cell Carcinoma Pathogenesis.Frontiers in genetics · 2019Article
- Expression and significance of the Hedgehog signal transduction pathway in oxygen-induced retinal neovascularization in mice.Drug design, development and therapy · 2018Article
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Authors and funding
3 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Since hedgehog (HH)/Gli1 that contributes to cancer proliferation and metastasis has been masked for decades, the signaling pathway was investigated about its exact role in proliferation and metastasis of cutaneous squamous cell carcinoma (SCC). Sonic hedgehog homolog (Shh), GLI family zinc finger 1 (Gli1), and vascular endothelial growth factor (VEGF) expressions in cutaneous SCC tissues were analyzed with immunohistochemistry, and their correlations with cutaneous SCC patients' prognosis were conducted with Kaplan-Meier curve. Regarding in vitro studies, effects of the HH signaling pathway, and cyclopamine on patched 1 (Ptch1), smoothened/frizzled class receptor (Smo) and VEGF expressions were assessed in A431 cells based on western blot and quantitative real-time polymerase chain reaction (qRT-PCR). Besides, Cell Counting Kit-8 (CCK-8) assay was implemented to evaluate cell proliferation, while wound-healing assay and transwell assay were performed to assess cell migration and invasion, respectively. Mice models were also established to observe effects of Gli1 on tumor diversity and incidence during a period of 20 weeks. Positively expressed VEGF, Gli1, and Shh proteins in cutaneous SCC tissues were correlated with poor survival of patients (P < 0.05). Besides, Gli1 messenger RNA (mRNA) and VEGF mRNA were observed to be significantly over-expressed in A431 cells (P < 0.05), and they were associated with incremental cell proliferation, invasiveness, and migration, which can be reversed by the interference of VEGF siRNA. Furthermore, cyclopamine treatment could induce inhibition of cell proliferation, invasiveness, and migration and suppression of Smo, Gli1, and VEGF expressions. The mice models also confirmed that Gli1 could significantly induce rise of tumor incidence and tumor diversity, while cyclopamine statistically relieved this transformation (P < 0.05). Abnormal activation of the HH signaling pathway plays critical roles in development of cutaneous SCC either in vivo or in vitro.
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