ArticleOxidative medicine and cellular longevity2022
IPO5 Mediates EMT and Promotes Esophageal Cancer Development through the RAS-ERK Pathway.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 17 citations in OpenAlex.
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- Transcriptomics-based analysis of key genes and potential mechanism and therapeutic agents in cadmium-induced esophageal squamous cell carcinoma progression.Scientific reports · 2025Article
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- The nuclear import receptor importin-7 targets HPV from the Golgi to the nucleus to promote infection.Science advances · 2025Article
- The nuclear transport factor IPO5 revealed as a critical mediator of male germline development†.Biology of reproduction · 2025Article
- Integrative analysis of molecular mechanisms in prostate cancer via single-cell RNA sequencing and weighted gene co-expression network analysis.Scientific reports · 2025Article
- Nitric oxide synthase 1 inhibits the progression of esophageal cancer through interacting with nitric oxide synthase 1 adaptor protein.World journal of gastrointestinal oncology · 2025Article
- The predictive value of necroptosis-related lncRNAs in prostate cancer prognosis and their potential to distinguish between cold and hot tumors.Frontiers in cell and developmental biology · 2025Article
- FUT6 Suppresses the Proliferation, Migration, Invasion, and Epithelial-Mesenchymal Transition of Esophageal Carcinoma Cells via the Epidermal Growth Factor Receptor/Extracellular Signal-Regulated Kinase Signaling Pathway.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2024Article
- NUP43 promotes PD-L1/nPD-L1/PD-L1 feedback loop via TM4SF1/JAK/STAT3 pathway in colorectal cancer progression and metastatsis.Cell death discovery · 2024Article
- Mechanism of lncRNA SNHG16 on kidney clear cell carcinoma cells by targeting miR-506-3p/ETS1/RAS/ERK molecular axis.Heliyon · 2024Article
- TRIM9 Interacts with ZEB1 to Suppress Esophageal Cancer by Promoting ZEB1 Protein Degradation via the UPP Pathway.BioMed research international · 2023Article
- Establishment and Analysis of an Artificial Neural Network Model for Early Detection of Polycystic Ovary Syndrome Using Machine Learning Techniques.Journal of inflammation research · 2023Article
- Differences in genome, transcriptome, miRNAome, and methylome in synchronous and metachronous liver metastasis of colorectal cancer.Frontiers in oncology · 2023Article
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8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Objective: In the development of many tumors, IPO5, as a member of the nuclear transporter family, exerts a significant function. Also, IPO5 is used as a therapeutic target for tumors based on some reports. By studying IPO5 expression in esophageal cancer tissues, the mechanism associated with IPO5 improving esophageal cancer development was explored in this study. Methods: To gain differentially expressed genes, this study utilized mRNA microarray and TCGA database for comprehensive analysis of esophageal cancer tissues and normal esophageal cancer tissues, and then the differentially expressed gene IPO5 was screened by us. To assess esophageal cancer patients' prognosis, this study also applied the Kaplan-Meier analysis, and we also conducted the GSEA enrichment analysis to investigate IPO5-related signaling pathways. This study performed TISIDB and TIMER online analysis tools to study the correlation between IPO5 and immune regulation and infiltration. We took specimens of esophageal cancer from patients and detected the expression of IPO5 in tumor and normal tissues by immunohistochemistry. The IPO5 gene-silenced esophageal cancer cell model was constructed by lentivirus transfection. Through the Transwell invasion assay, CCK-8 assay, and cell scratch assay, this study investigated the effects of IPO5 on cell propagation, invasion, and transfer. What is more, we identified the influences of IPO5 on the cell cycle through flow cytometry and established a subcutaneous tumor-forming model in nude mice. Immunohistochemistry was used to verify the expression of KI-67, and this study detected the modifications of cell pathway-related proteins using Western blot and applied EMT-related proteins to explain the mechanism of esophageal cancer induced by IPO5. Results: According to database survival analysis, IPO5 high-expression patients had shorter disease-free survival than IPO5 low-expression patients. Compared to normal tissues, the IPO5 expression in cancer tissues was significantly higher in clinical trials ( Conclusion: In esophageal cancer, IPO5 is highly expressed and correlates with survival rate. Esophageal cancer cell growth and migration were significantly affected by the inhibition of IPO5 in vitro and in vivo. IPO5 mediates EMT using the RAS-ERK signaling pathway activation and promotes esophageal cancer cell development in vivo and in vitro.
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