ArticleMolecular carcinogenesis2017
Copy number variation, increased gene expression, and molecular mechanisms of neurofascin in lung cancer.
Article in Molecular carcinogenesis, 2017. 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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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
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- Integrated bioinformatics and experiments reveal the roles and driving forces for HSF1 in colorectal cancer.Bioengineered · 2022Article
- Multiclass Cancer Prediction Based on Copy Number Variation Using Deep Learning.Computational intelligence and neuroscience · 2022Article
- STIL Acts as an Oncogenetic Driver in a Primary Cilia-Dependent Manner in Human Cancer.Frontiers in cell and developmental biology · 2022Article
- Identification ofPharmacogenomics and personalized medicine · 2022Article
- Multi-Omics Analysis Detects Novel Prognostic Subgroups of Breast Cancer.Frontiers in genetics · 2020Article
- Copy number variation is highly correlated with differential gene expression: a pan-cancer study.BMC medical genetics · 2019Article
- Article
- Genomic and regulatory characteristics of significant transcription factors in colorectal cancer metastasis.Scientific reports · 2018Article
- Copy number variation, increased gene expression, and molecular mechanisms of neurofascin in lung cancer.Molecular carcinogenesis · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastasis and cell adhesion are key aspects of cancer progression. Neurofascin (NFASC) is a member of the immunoglobulin superfamily of adhesion molecules and, while studies on NFASC are inadequate, other members have been indicated pivotal roles in cancer progression and metastasis. This study aimed at increasing the knowledge on the involvement of adhesion molecules in lung cancer progression by studying the regulation and role of NFASC in non-small cell lung cancer (NSCLC). Here, copy number variations in the NFASC gene were analyzed in tumor and non-tumorous lung tissues of 204 NSCLC patients. Frequent gene amplifications (OR = 4.50, 95%CI: 2.27-8.92, P ≤ 0.001) and increased expression of NFASC (P = 0.034) were identified in tumors of NSCLC patients. Furthermore, molecular mechanisms of NFASC in lung cancer progression were evaluated by investigating the effects of NFASC silencing on cell proliferation, viability, migration, and invasion using siRNA technology in four NSCLC cell lines. Silencing of NFASC did not affect cell proliferation or viability but rather decreased NSCLC cell migration (P ≤ 0.001) and led to morphological changes, rearrangements in the actin cytoskeleton and changes in F-actin networks in migrating NSCLC cell lines. This study is the first to report frequent copy number gain and increased expression of NFASC in NSCLC. Moreover, these data suggest that NFASC is a novel regulator of NSCLC cell motility and support a role of NFASC in the regulation of NSCLC progression.
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