ArticleBone & joint research2021
GNAQ knockdown promotes bone metastasis through epithelial-mesenchymal transition in lung cancer cells.
Article in Bone & joint research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.
- Prognostic role of lymph node regression in patients with esophageal cancer undergoing neoadjuvant therapy.Pathology oncology research : POR · 2024Pooled it
- Vascular Ossification in the Developing Brain: A Case Study of Pediatric Sturge Weber Syndrome.Neuroscience bulletin · 2025Article
- Genomic alterations in the stepwise progression from normal mucosa to metastasizing oral squamous cell carcinoma.Frontiers in oncology · 2024Article
- New insights into non-small cell lung cancer bone metastasis: mechanisms and therapies.International journal of biological sciences · 2024Review
- GNAQ-Regulated ZO-1 and ZO-2 Act as Tumor Suppressors by Modulating EMT Potential and Tumor-Repressive Microenvironment in Lung Cancer.International journal of molecular sciences · 2023Article
- Cyclin D1 mediates pain behaviour in a rat model of breast cancer-induced bone pain by a mechanism involving regulation of the proliferation of spinal microglia.Bone & joint research · 2022Article
- Exploration of the Shared Gene and Molecular Mechanisms Between Endometriosis and Recurrent Pregnancy Loss.Frontiers in veterinary science · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsBone metastasis ultimately occurs due to a complex multistep process, during which the interactions between cancer cells and bone microenvironment play important roles. Prior to colonization of the bone, cancer cells must succeed through a series of steps that will allow them to gain migratory and invasive properties; epithelial-to-mesenchymal transition (EMT) is known to be integral here. The aim of this study was to determine the effects of G protein subunit alpha Q (GNAQ) on the mechanisms underlying bone metastasis through EMT pathway.
methodsA total of 80 tissue samples from patients who were surgically treated during January 2012 to December 2014 were used in the present study. Comparative gene analysis revealed that the GNAQ was more frequently altered in metastatic bone lesions than in primary tumour sites in lung cancer patients. We investigated the effects of GNAQ on cell proliferation, migration, EMT, and stem cell transformation using lung cancer cells with GNAQ-knockdown. A xenograft mouse model tested the effect of GNAQ using micro-CT analyses and histological analyses.
resultsGNAQ-knockdown showed down-regulation of tumour growth through mitogen-activated protein kinase (MAPK) signalling in lung cancer cells, but not increased apoptosis. We found that GNAQ-knockdown induced EMT and promoted invasiveness. GNAQ-knockdown cells injected into the bone marrow of murine tibia induced tumour growth and bone-to-lung metastasis, whereas it did not in control mice. Moreover, the knockdown of GNAQ enhanced cancer stem cell-like properties in lung cancer cells, which resulted in the development of resistance to chemotherapy.
conclusionThe present study reveals that the GNAQ-knockdown induced cancer stem cell-like properties. Cite this article:
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