ArticleAmerican journal of cancer research2018
Overexpression of golgi membrane protein 1 promotes non-small-cell carcinoma aggressiveness by regulating the matrix metallopeptidase 13.
Article in American journal of cancer research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- New proteomic signature in circulating extracellular vesicles from tumor-draining and peripheral veins of patients with lung adenocarcinoma.Cancer cell international · 2026Article
- The role of GP73 in predicting overall survival and chemotherapy response in locally advanced gastric cancer: a retrospective cohort study.BMC gastroenterology · 2026Article
- Lung microbiome dynamics in health and lung cancer.Microbial genomics · 2025Review
- GCC2 promotes non-small cell lung cancer progression by maintaining Golgi apparatus integrity and stimulating EGFR signaling pathways.Scientific reports · 2024Article
- Classification prediction of early pulmonary nodes based on weighted gene correlation network analysis and machine learning.Journal of cancer research and clinical oncology · 2023Article
- Cell-cycle dependent nuclear gene delivery enhances the effects of E-cadherin against tumor invasion and metastasis.Signal transduction and targeted therapy · 2023Article
- Clinical significance of golgi protein-73 as a diagnostic marker for Egyptian patients with colorectal cancer: Preliminary study.Cancer reports (Hoboken, N.J.) · 2021Article
- Article
- GOLM1 predicts poor prognosis of patients with NSCLC and is associated with the proliferation and chemo-sensitivity of cisplatin in NSCLC cells: bioinformatics analysis and laboratory validation.Journal of bioenergetics and biomembranes · 2021Article
- The functional landscape of Golgi membrane protein 1 (GOLM1) phosphoproteome reveal GOLM1 regulating P53 that promotes malignancy.Cell death discovery · 2021Article
- Golgi Phosphoprotein 73: The Driver of Epithelial-Mesenchymal Transition in Cancer.Frontiers in oncology · 2021Review
- Golgi protein 73, hepatocellular carcinoma and other types of cancers.Liver research (Beijing, China) · 2020Article
- LINC00992 contributes to the oncogenic phenotypes in prostate cancer via targeting miR-3935 and augmenting GOLM1 expression.BMC cancer · 2020Article
- Effects of hub genes on the clinicopathological and prognostic features of lung adenocarcinoma.Oncology letters · 2020Article
- Knockdown of lncRNA PCAT1 Enhances Radiosensitivity of Cervical Cancer by Regulating miR-128/GOLM1 Axis.OncoTargets and therapy · 2020Article
- MicroRNA-374b inhibits the tumor growth and promotes apoptosis in non-small cell lung cancer tissue through the p38/ERK signaling pathway by targeting JAM-2.Journal of thoracic disease · 2018Article
- Research progress on GP73 in malignant tumors.OncoTargets and therapy · 2018Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small-cell carcinoma (NSCLC) is one of the most lethal malignancies of lung cancers and its prognosis remains dismal due to the paucity of effective therapeutic targets. Recent reports show that Golgi membrane protein 1 (GOLM1) is highly expressed in a variety of tumor cells, functions as a negative regulator of T cells and then promotes tumor progression. However, its expression and role in NSCLC remain unclear. Herein, we showed that GOLM1 was markedly up-regulated in NSCLC cell lines and clinical tissues. Clinically, NSCLC patients with high expression of GOLM1 had shorter overall survival (OS) and high GOLM1 expression in tumor samples was significantly related to malignant phenotype, such as lymph node metastasis and high tumor stage. Ectopic expression of GOLM1 in NSCLC cells induced epithelial-to-mesenchymal transition (EMT) and promoted proliferation, migration, and invasion of NSCLC cells in vitro. Furthermore, GOLM1 overexpressing significantly promoted the tumorigenicity of NSCLC cells in vivo whereas silencing endogenous GOLM1 caused an opposite outcome. Moreover, we demonstrated that GOLM1 enhanced NSCLC aggressiveness by activating matrix metalloproteinase-13 (MMP13) signaling. Together, our results provided new evidence that GOLM1 overexpression promoted the progression of NSCLC and might represent a novel therapeutic target for its treatment.
Indexed as
Identifiers
29637008PMC5883103W2946179714What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.