ArticleOncoTargets and therapy2018
Rab18 overexpression promotes proliferation and chemoresistance through regulation of mitochondrial function in human gastric cancer.
Article in OncoTargets and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Ferroptosis and Ferroptosis-related autophagy: new therapeutic targets for gastric cancer.American journal of cancer research · 2026Review
- 2'3'-cGAMP interactome identifies 2'3'-cGAMP/Rab18/FosB signaling in cell migration control independent of innate immunity.Science advances · 2024Article
- Function and regulation of Rab GTPases in cancers.Cell biology and toxicology · 2024Review
- Autophagy modulators influence the content of important signalling molecules in PS-positive extracellular vesicles.Cell communication and signaling : CCS · 2023Article
- Yang-xin-xue keli exerts therapeutic effectsFrontiers in pharmacology · 2022Article
- Rab18 interacted with V-set and immunoglobulin domain-containing 4 (VSIG4) to involve in the apoptosis of glioma and the sensitivity to temozolomide.Bioengineered · 2021Article
- Characterization of aNAR cancer · 2021Article
- miR-455 Inhibits the Viability and Invasion by Targeting RAB18 in Hepatocellular Carcinoma.Journal of oncology · 2021Article
- Rab18 binds to classical swine fever virus NS5A and mediates viral replication and assembly in swine umbilical vein endothelial cells.Virulence · 2020Article
- Pan-cancer driver copy number alterations identified by joint expression/CNA data analysis.Scientific reports · 2020Article
- Evidence for Enhanced Exosome Production in Aromatase Inhibitor-Resistant Breast Cancer Cells.International journal of molecular sciences · 2020Article
- Comprehensive analysis of the value of RAB family genes in prognosis of breast invasive carcinoma.Bioscience reports · 2020Article
- Rab GTPases: Emerging Oncogenes and Tumor Suppressive Regulators for the Editing of Survival Pathways in Cancer.Cancers · 2020Review
- Rab18 Regulates Proliferation, Invasion and Cisplatin Sensitivity Through STAT3 Signaling in Head and Neck Squamous Cell Carcinoma.OncoTargets and therapy · 2020Article
- miR-145-5p Acts as a Novel Tumor Suppressor in Hepatocellular Carcinoma Through Targeting RAB18.Technology in cancer research & treatment · 2019Article
Corrections and comments
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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
backgroundDysregulation of Rab18 has been implicated in human cancers. However, its clinical significance and biological function in gastric cancer have not been investigated.
methodsWe examined Rab18 expression in gastric cancer tissues using immunohistochemistry. We used SNU-1 and AGS cell lines for plasmid and siRNA transfection respectively. MTT, colony formation assay, cell cycle analysis, matrigel invasion, wound healing assay, AnnexinV/PI analysis and western blotting were used to examine the biological effect and mechanism of Rab18 in gastric cancer cell lines.
resultsRab18 protein expression was upregulated in gastric cancer tissues and this correlated with advanced stage and poor prognosis. Rab18 overexpression promoted proliferation in vitro and in vivo. Cell cycle analysis showed that Rab18 overexpression upregulated, while its depletion downregulated S phase percentage. Matrigel invasion and wound healing assays indicated that Rab18 positively regulated SNU-1 cell invasion and migration while its knockdown inhibited AGS cell invasion and migration. Rab18 maintained cell viability and downregulated apoptosis after cisplatin treatment, with upregulated mitochondrial membrane potential and downregulated mitochondrial reactive oxygen species (ROS) production. Rab18 overexpression upregulated p-Rb, survivin while downregulated cytochrome c, cleaved caspase-3 and cleaved PARP.
conclusionIn conclusion, our results indicate that Rab18 promoted gastric cancer growth and chemoresistance, possibly through regulation of mitochondrial function and survivin.
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