AI Article Synopsis
- Non-small cell lung cancer (NSCLC) is a major cause of cancer-related deaths, but its progression mechanisms are still not completely understood.
- A study involving 347 NSCLC patients found that high levels of STYK1 and low levels of SPINT2 are linked to worse patient outcomes, tumor growth, and spread.
- STYK1 promotes cancer cell activity by decreasing SPINT2 levels, suggesting that targeting both proteins could be a promising new treatment approach for NSCLC.
Article Abstract
Non-small cell lung cancer (NSCLC) is the leading cause of cancer deaths worldwide. However, the molecular mechanisms underlying NSCLC progression remains not fully understood. In this study, 347 patients with complete clinicopathologic characteristics who underwent NSCLC surgery were recruited for the investigation. We verified that elevated serine threonine tyrosine kinase 1 (STYK1) or decreased serine peptidase inhibitor Kunitz type 2 (SPINT2/HAI-2) expression significantly correlated with poor prognosis, tumor invasion, and metastasis of NSCLC patients. STYK1 overexpression promoted NSCLC cells proliferation, migration, and invasion. STYK1 also induced epithelial-mesenchymal transition by E-cadherin downregulation and Snail upregulation. Moreover, RNA-seq, quantitative polymerase chain reaction (qRT-PCR), and western blot analyses confirmed that STYK1 overexpression significantly decreased the SPINT2 level in NSCLC cells, and SPINT2 overexpression obviously reversed STYK1-mediated NSCLC progression both in vitro and in vivo. Further survival analyses showed that NSCLC patients with high STYK1 level and low SPINT2 level had the worst prognosis and survival. These results indicated that STYK1 facilitated NSCLC progression via reducing SPINT2 expression. Therefore, targeting STYK1 and SPINT2 may be a novel therapeutic strategy for NSCLC.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6547759 | PMC |
| http://dx.doi.org/10.1038/s41419-019-1659-1 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Impact of co-mutations and transcriptional signatures in non-small cell lung cancer patients treated with adagrasib in the KRYSTAL-1 trial.
Clin Cancer Res
January 2025
The University of Texas MD Anderson Cancer Center, Houston, TX, United States.
Background: KRAS inhibitors are revolutionizing the treatment of NSCLC, but clinico-genomic determinants of treatment efficacy warrant continued exploration.
Methods: Patients with advanced KRASG12C-mutant NSCLC treated with adagrasib (KRYSTAL-1-NCT03785249) were included in the analysis. Pre-treatment NGS data were collected per protocol.
circ-ZEB1 Enhances NSCLC Metastasis and Proliferation by Modulating the miR-491-5p/EIF5A Axis.
Anal Cell Pathol (Amst)
January 2025
Department of General Practice, Renji Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China.
Circular RNAs (circRNAs), covalently closed single-stranded RNAs, have been implicated in cancer progression. A previous investigation revealed that circ-ZEB1 is expressed abnormally in liver cancer. However, the roles of circ-ZEB1 in non-small cell lung cancer (NSCLC) are unknown.
View Article and Find Full Text PDFLINC00323 knockdown suppresses the proliferation, migration, and vascular mimicry of non-small cell lung cancer cells by promoting ubiquitinated degradation of AKAP1.
Noncoding RNA Res
April 2025
Department of Traditional Chinese Medicine, Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Guangdong-Hong Kong Joint Laboratory for RNA Medicine, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, Guangdong, China.
Background: LINC00323, a new long noncoding RNA, is aberrantly expressed in several cancers. However, the expression, function, and mechanism of LINC00323 in non-small cell lung cancer (NSCLC) are unclear.
Methods: In the present study, LINC00323, VEGFA, microvessel density (MVD), and AKAP1 levels were confirmed in NSCLC tissues.
Discovery of novel PDGFR inhibitors targeting non-small cell lung cancer using a multistep machine learning assisted hybrid virtual screening approach.
RSC Adv
January 2025
Innovative Informatica Technologies Hyderabad Telangana India.
Non-Small Cell Lung Cancer (NSCLC) is a formidable global health challenge, responsible for the majority of cancer-related deaths worldwide. The Platelet-Derived Growth Factor Receptor (PDGFR) has emerged as a promising therapeutic target in NSCLC, given its crucial involvement in cell growth, proliferation, angiogenesis, and tumor progression. Among PDGFR inhibitors, avapritinib has garnered attention due to its selective activity against mutant forms of PDGFR, particularly PDGFRA D842V and KIT exon 17 D816V, linked to resistance against conventional tyrosine kinase inhibitors.
View Article and Find Full Text PDFCircENTPD7 affects the immune escape of non‑small cell lung cancer cells by modulating the IGF2BP2/PD‑L1 axis.
Oncol Lett
March 2025
Department of Radiotherapy, Affiliated Cancer Hospital and Institute of Guangzhou Medical University, Guangzhou, Guangdong 510095, P.R. China.
Programmed death ligand 1 (PD-L1), an important immune checkpoint molecule, is abnormally activated in non-small cell lung cancer (NSCLC), which can interact with programmed death 1 to aid cancer cells in evading immune surveillance. Furthermore, tumor driver genes may be involved in the occurrence and development of NSCLC and have a potential role in PD-L1-mediated immune escape mechanisms. Therefore, the present study aimed to assess the behavioral and regulatory mechanisms by which circular RNA ENTPD7 (circENTPD7; hsa_circ_0019421) induces an immune response in the progression of NSCLC cells.
View Article and Find Full Text PDFWant 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!