ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2018
Glycoprotein nonmetastatic melanoma protein B accelerates tumorigenesis of cervical cancer in vitro by regulating the Wnt/β-catenin pathway.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Tumor-expressed GPNMB orchestrates Siglec-9Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- LncRNA CCAT1 decreases the sensitivity to doxorubicin in lung cancer cells by regulating miR-181a/CPEB2 axis.Medical oncology (Northwood, London, England) · 2025Article
- AUP1 transcriptionally activated by KDM5B reprograms lipid metabolism to promote the malignant progression of cervical cancer.International journal of oncology · 2024Article
- Identification of GPNMB in endometrial cancer based on pan-cancer analysis and in vitro validation.Discover oncology · 2024Article
- Gefitinib suppresses cervical cancer progression by inhibiting cell cycle progression and epithelial-mesenchymal transition.Experimental and therapeutic medicine · 2019Article
- Role of the kringle-like domain in glycoprotein NMB for its tumorigenic potential.Cancer science · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer is one of the most common cancers among women around the world. However, the underlying mechanism involved in cervical cancer progression is incompletely known. In the present study, we determined the role of glycoprotein nonmetastatic melanoma protein B (GPNMB) in tumorigenesis of cervical cancer. According to the GEO database, we found that GPNMB expression was significantly higher in cervical cancer than in normal cervix epithelium. A similar pattern was observed in GPNMB expression in cultured cervical cancer cells and normal cervical epithelial cells. Compared with the control, GPNMB knockdown significantly decreased the proliferation and migration capacity, but enhanced the apoptosis capacity of SiHa and HeLa cells. Additionally, the activity of MMP-2 and MMP-9 were aberrantly increased in SiHa and HeLa cells compared with normal cervical epithelial cells, whereas their activities were strongly inhibited by GPNMB siRNA. Furthermore, Wnt/β-catenin signaling was activated by GPNMB in SiHa and HeLa cells. Increased MMP-2/MMP-9 expression was suppressed by Dkk-1, inhibitor of Wnt/β-catenin signaling, while it was enhanced by stimulator BIO. The proliferation, migration, and apoptosis capacity of HeLa cells were found to be affected by Dkk-1 and BIO to different extents. In conclusion, we demonstrated that GPNMB contributed to the tumorigenesis of cervical cancer, at least in part, by regulating MMP-2/MMP-9 activity in tumor cells via activation of canonical Wnt/β-catenin signaling. This might be a potential therapeutic target for treating human cervical cancer.
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