Vasohibin-1 (VASH1) is a newly discovered angiogenesis inhibitor that is specifically expressed in human vascular endothelial cells in response to vascular endothelial growth factor and fibroblast growth factor-2. This study aimed to evaluate the expression of VASH1 in non-small cell lung cancer (NSCLC) and correlates its expression with the clinicopathological parameters and prognosis of the disease. Immunohistochemical analysis was used to determine the expression of VASH1 in NSCLC tissue and adjacent normal tissue from 84 patients. The relationship between VASH1 expression and clinicopathological indicators was examined with the chi-squared test. Moreover, the survival rate was calculated with the Kaplan-Meier survivor curve. Finally, the correlation between the indicators and patient survival was estimated with Cox analysis. VASH1 was high expressed in 63.1% of NSCLC tissues versus 21.4% of adjacent tissues (P < 0.01). High VASH1 expression in NSCLC tissue was correlated with clinicopathological features including lymph node status (P = 0.024) and TNM stage (P = 0.036). The Kaplan-Meier curve indicated that the patients with high VASH1 expression had significantly shorter survival than those with low VASH1 expression. In the multivariate Cox regression model, high VASH1 expression was identified as an independent prognostic factor for patients with NSCLC. High VASH1 expression is predictive of poor prognosis of NSCLC, implying that VASH1 may be a promising new target for targeted therapies for NSCLC.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1007/s12032-014-0963-y | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
circSIRT2/miR-542-3p/VASH1 axis regulates endothelial-to-mesenchymal transition (EndMT) in subretinal fibrosis in age-related macular degeneration models.
Aging Cell
January 2025
Department of Ophthalmology, Shanghai General Hospital, Shanghai Jiao Tong University, School of Medicine, Shanghai, China.
Neovascular age-related macular degeneration (nAMD), characterized by choroidal neovascularization (CNV), is one of the leading causes of severe visual impairment and irreversible vision loss around the world. Subretinal fibrosis (SRF) contributes to the incomplete response to anti-vascular endothelial growth factor (VEGF) treatment and is one of the main reasons for long-term poor visual outcomes in nAMD. Reducing SRF is urgently needed in the anti-VEGF era.
View Article and Find Full Text PDFForced Vasohibin-1 Expression Increases Paclitaxel Sensitivity of Ovarian Cancer by Inhibiting Microtubule Activity.
Cancer Rep (Hoboken)
December 2024
Department of Obstetrics and Gynecology, School of Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Background: Vasohibin-1 (VASH1), an angiogenic inhibitor, exhibits tubulin carboxypeptidase activity, which is involved in microtubule functions. Paclitaxel, the core chemotherapeutic agent for ovarian cancer chemotherapy, has a point of action on microtubules and may interact with VASH1.
Aims: To examine the influence of VASH1 on intracellular tubulin detyrosination status, cyclin B1 expression, and paclitaxel chemosensitivity using VASH1-overexpressing ovarian cancer cell lines.
Evaluation of vascular peroxidase 1, humanin, MOTS-c and miR-200c expression levels in untreated preeclampsia patients.
Mol Biol Rep
December 2024
Department of Medical Biochemistry, Cerrahpasa Faculty of Medicine, Istanbul University-Cerrahpasa, Istanbul, Turkey.
Article Synopsis
- The study investigates the levels of Vascular Peroxidase 1 (VPO1), humanin, and MOTS-c in untreated preeclamptic pregnancies, focusing on their relationship with miR-200c expression and comparing these findings to endoglin levels.
- Blood samples from preeclamptic patients showed significantly elevated levels of endoglin, VPO1, and miR-200c, while MOTS-c levels were reduced; humanin levels did not differ significantly.
- A strong positive correlation was found between endoglin and VPO1, suggesting that these molecular changes may play a role in the pathogenesis of preeclampsia and contribute to endothelial dysfunction.
Develop a Novel Signature to Predict the Survival and Affect the Immune Microenvironment of Osteosarcoma Patients: Anoikis-Related Genes.
J Immunol Res
October 2024
Department of Joint Surgery, HongHui Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Objective: Osteosarcoma (OS) represents a prevalent primary bone neoplasm predominantly affecting the pediatric and adolescent populations, presenting a considerable challenge to human health. The objective of this investigation is to develop a prognostic model centered on anoikis-related genes (ARGs), with the aim of accurately forecasting the survival outcomes of individuals diagnosed with OS and offering insights into modulating the immune microenvironment.
Methods: The study's training cohort comprised 86 OS patients sourced from The Cancer Genome Atlas database, while the validation cohort consisted of 53 OS patients extracted from the Gene Expression Omnibus database.
A Multi-Omics Approach to Defining Target Organ Injury in Youth with Primary Hypertension.
bioRxiv
June 2024
Department of Internal Medicine, Division of Cardiovascular Health and Diseases, Center for Cardiovascular Research, University of Cincinnati College of Medicine, Cincinnati, OH.
Article Synopsis
- Primary hypertension in children can lead to increased cardiovascular risks as they grow into adults, making early studies crucial for understanding organ damage.
- A study involving 132 youths showed significant correlations between blood pressure levels, gene expression, and molecular profiles, highlighting distinct biological changes in those with high blood pressure.
- Findings suggest that mechanisms behind elevated blood pressure could involve issues with blood vessel growth and tissue breakdown, offering potential targets for intervention in preventing long-term cardiovascular damage.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!