ArticleOncotarget2016
WW45, a Gli1 binding protein, negatively regulated Hedgehog signaling in lung cancer.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Glioma-associated oncogene homolog 1 in breast invasive carcinoma: a comprehensive bioinformatic analysis and experimental validation.Frontiers in cell and developmental biology · 2024Article
- Impaired Expression of the Salvador Homolog-1 Gene Is Associated with the Development and Progression of Colorectal Cancer.Cancers · 2023Article
- The tumor suppressor role of salvador family WW domain-containing protein 1 (SAV1): one of the key pieces of the tumor puzzle.Journal of cancer research and clinical oncology · 2021Review
- WW45 inhibits breast cancer cell proliferation by the Hedgehog signaling pathway.American journal of translational research · 2021Article
- RNA-binding protein Musashi2 regulates Hippo signaling via SAV1 and MOB1 in pancreatic cancer.Medical oncology (Northwood, London, England) · 2020Article
- Correction of the tumor suppressor Salvador homolog-1 deficiency in tumors by lycorine as a new strategy in lung cancer therapy.Cell death & disease · 2020Article
- Role and inhibition of GLI1 protein in cancer.Lung Cancer (Auckland, N.Z.) · 2018Review
- Activating transcription factor 3 promotes malignance of lung cancer cells in vitro.Thoracic cancer · 2017Article
- The RNA-binding protein Sam68 is critical for non-small cell lung cancer cell proliferation by regulating Wnt/β-catenin pathway.International journal of clinical and experimental pathology · 2017Article
- Weighted gene co-expression network analysis in identification of metastasis-related genes of lung squamous cell carcinoma based on the Cancer Genome Atlas database.Journal of thoracic disease · 2017Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over-expression of Gli1 is very common in lung cancer. However, the underlying molecular mechanism remains largely unknown. Here, using mass spectrum, we have identified WW45 as a binding partner of Gli1. WW45 interacted with Gli1, promoted its ubiquitination and inhibited the expression of its target genes. In the functional studies, WW45 inhibited the growth and migration of lung cancer cells. Knocking down the expression of WW45 promoted the growth and migration of lung cancer cells, which was rescued by down-regulation of Gli1. Moreover, over-expression of WW45 inhibited the tumorigenesis in a de novo lung cancer tumorigenesis mouse model (LKB-Ras) as well as the expression of Gli1. Also over-expression of WW45 improved the survival of these mice. In addition, the expression of WW45 was down-regulated in the clinical lung cancer samples, which was inversely correlated with the expression of Gli1. Taken together, this study demonstrated the suppressive roles of WW45 in lung cancer by inhibiting the Hedgehog/Gli1 signaling.
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