ArticleMedical science monitor : international medical journal of experimental and clinical research2016
High Expression of Rab-like 3 (Rabl3) is Associated with Poor Survival of Patients with Non-Small Cell Lung Cancer via Repression of MAPK8/9/10-Mediated Autophagy.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2016. 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, 31 citations in OpenAlex.
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- Knockdown of RABL3 suppresses the proliferation and invasion of oral squamous cell carcinoma through inactivating the FAK/AKT pathway.Journal of bioenergetics and biomembranes · 2021Article
- CircMED13L_012 promotes lung adenocarcinoma progression by upregulation of MAPK8 mediated by miR-433-3p.Cancer cell international · 2021Article
- circCOL1A1 Promotes the Progression of Gastric Cancer Cells through Sponging miR-145 to Enhance RABL3 Expression.Journal of immunology research · 2021Article
- Convergent network effects along the axis of gene expression during prostate cancer progression.Genome biology · 2020Article
- Identification of GIMAP7 and Rabl3 as Putative Biomarkers for Oral Squamous Cell Carcinoma Through Comparative Proteomic Approach.Pathology oncology research : POR · 2020Article
- Genetic and structural studies of RABL3 reveal an essential role in lymphoid development and function.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Epigenome-Wide Tobacco-Related Methylation Signature Identification and Their Multilevel Regulatory Network Inference for Lung Adenocarcinoma.BioMed research international · 2020Article
- Fighting Thyroid Cancer with Microgravity Research.International journal of molecular sciences · 2019Review
- RUFY3 Predicts Poor Prognosis and Promotes Metastasis through Epithelial-mesenchymal Transition in Lung Adenocarcinoma.Journal of Cancer · 2019Article
- Exogenous Let-7a-5p Induces A549 Lung Cancer Cell Death Through BCL2L1-Mediated PI3Kγ Signaling Pathway.Frontiers in oncology · 2019Article
- GSAE: an autoencoder with embedded gene-set nodes for genomics functional characterization.BMC systems biology · 2018Article
- Expression profiling analysis of autophagy-related genes in perineural invasion of cutaneous squamous cell carcinoma.Oncology letters · 2018Article
- Promotion of Cell Proliferation through Inhibition of Cell Autophagy Signalling Pathway by Rab3IP is Restrained by MicroRNA-532-3p in Gastric Cancer.Journal of Cancer · 2018Article
- Correlation Between Methylenetetrahydrofolate Reductase (MTHFR) C677T Polymorphisms and Pemetrexed Chemotherapy Efficacy/Toxicity in Non-Squamous Non-Small Cell Lung Cancer.Medical science monitor : international medical journal of experimental and clinical research · 2017Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Rab-like 3 (Rabl3) is a member of the Rab subfamily of small GTPases which are involved in controlling proliferation and vesicular trafficking. Recent studies suggest that Rab proteins might play a critical role in regulating cancer cell survival, but the underlying mechanisms remain largely unknown. MATERIAL AND METHODS We performed a bioinformatics analysis to examine the correlation between the expression level of Rabl3 and survival of non-small cell lung cancer (NSCLC) patients in three independent cohorts containing 484 patients. The function of Rabl3 was examined in NSCLC cell line A549 in vitro. Following Rabl3 knockdown, cells were stained with propidium iodine (PI) and Annexin V, followed by flow cytometry analysis (FACS) for cell death and autophagy induction. The activity of the MAPK signaling pathway was assessed by Western blotting of different MAPK phosphorylations, and modulated with different chemical inhibitors. RESULTS High expression of Rabl3 was significantly correlated with poor survival in all three independent NSCLC cohorts. In line with this result, Rabl3 was frequently overexpressed in lung cancer cell lines as compared with normal lung fibroblast cell lines. Knockdown of Rabl3 in lung cancer cells significantly enhanced cell death accompanied with autophagy induction, as evidenced by an increased level of autophagy marker LC3-II. Interestingly, Rabl3 knockdown was associated with enhanced activation of MAPK8/9/10 but not MAPK11/12/13/14. Treatment of MAPK8/9/10-specific inhibitor SP600125, but not MAPK11/12/13/14-specific inhibitor SB203580, largely abolished Rabl3 knockdown-induced LC3-I/LC3-II conversion and autophagic cell death. CONCLUSIONS Together, these results suggest that high expression of Rabl3 might inhibit cell death in NSCLCs via repression of MAPK8/9/10-mediated autophagy.
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