ArticleCancer biomarkers : section A of Disease markers2019
Golgi phosphoprotein 3 (GOLPH3) promotes endometrial carcinoma cell invasion and migration by regulating the epithelial-mesenchymal transition.
Article in Cancer biomarkers : section A of Disease markers, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- [Preliminary Study on Drug-Loaded Chondroitin Sulfate-Modified Micelles Targeting Golgi Apparatus in Tumor Cells for the Treatment of Tumor Metastasis].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2022Article
- Medroxyprogesterone Reverses Tolerable Dose Metformin-Induced Inhibition of Invasion via Matrix Metallopeptidase-9 and Transforming Growth Factor-β1 in KLE Endometrial Cancer Cells.Journal of clinical medicine · 2020Article
- [Golgi phosphoprotein 3 overexpression inhibits paclitaxel-induced apoptosis in HeLa cells by promoting autophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
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9 authors at 2 institutions in 1 country.
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Abstract
backgroundGolgi phosphoprotein 3 (GOLPH3) is a novel oncogene overexpressed in several human cancers, but specific contributions to endometrial carcinoma (EC) have not been examined. The aims of this study were to evaluate the GOLPH3 expression in EC and investigate its functions in EC cell proliferation, migration, and survival.
methodsThe expression levels of GOLPH3 in EC patient samples and EC cell lines (HEC-1A, KLE, RL95-2, and Ishikawa) were examined using qRT-PCR, western blotting and immunohistochemistry. Further, EC cell lines with either ectopic GOLPH3 overexpression or knockdown were established, and the effects on proliferation, apoptosis, invasion, and migration were investigated in vitro using cell viability and transwell assays and in mice following cell injection.
resultsCompared to adjacent non-cancerous tissues, expression of GOLPH3 was significantly upregulated in EC tissues (P< 0.05), and the expression level of GOPLPH3 was related to the grade of the tumor (P< 0.05). The expression of GOLPH3 was also higher in all four EC cell lines than endometrial stromal cells (ESCs) (P< 0.05). Moreover, GOLPH3 expression was greater in EC cell lines with high invasive capacity than in non-invasive EC cells (P< 0.05). Knockdown of GOLPH3 inhibited EC cell proliferation and increased cell apoptosis in vitro. Further, knockdown of GOLPH3 also inhibited EC cell invasion and migration in vitro and in vivo by regulating the epithelial-mesenchymal transition (EMT). Conversely, GOLPH3 overexpression promoted proliferation and migration.
conclusionsThe present study provides evidence that GOLPH3 promotes EMT and metastasis of EC cells and predicts the risk of EC progression, highlighting its potential as a therapeutic target for this malignancy.
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