ArticleOncology letters2018
The function of FAK/CCDC80/E-cadherin pathway in the regulation of B16F10 cell migration.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Flexible integration of spatial and expression information for precise spot embedding via ZINB-based graph-enhanced autoencoder.Communications biology · 2025Article
- Si-Wu-Tang improves liver fibrosis by restoring liver sinusoidal endothelial cell functionality and reducing communication with hepatic stellate cells.Chinese medicine · 2024Article
- Silencing immune-infiltrating biomarker CCDC80 inhibits malignant characterization and tumor formation in gastric cancer.BMC cancer · 2024Article
- Lactate Metabolism Subtypes Analysis Reveals CCDC80 as a Novel Prognostic Biomarker in Gastric Cancer.Journal of Cancer · 2024Article
- Phenotype screens of murine pancreatic cancer identify a Tgf-α-Ccl2-paxillin axis driving human-like neural invasion.The Journal of clinical investigation · 2023Article
- Article
- Integrative analysis deciphers the heterogeneity of cancer-associated fibroblast and implications on clinical outcomes in ovarian cancers.Computational and structural biotechnology journal · 2022Article
- Downregulation of the Coiled-Coil Domain Containing 80 and Its Perspective Mechanisms in Ovarian Carcinoma: A Comprehensive Study.International journal of genomics · 2021Article
- A Tumor Progression Related 7-Gene Signature Indicates Prognosis and Tumor Immune Characteristics of Gastric Cancer.Frontiers in oncology · 2021Article
- Bioinformatics analysis and verification of molecular targets in ovarian cancer stem-like cells.Heliyon · 2020Article
- Inhibition of TGF-β signalling in combination with nal-IRI plus 5-Fluorouracil/Leucovorin suppresses invasion and prolongs survival in pancreatic tumour mouse models.Scientific reports · 2020Article
- A novel association of CCDC80 with gestational diabetes mellitus in pregnant women: a propensity score analysis from a case-control study.BMC pregnancy and childbirth · 2020Article
- Recombinant Expression and Bioactivity Characterization of TAT-Fused Thymosin β10.The protein journal · 2019Article
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
Focal adhesion kinase (FAK) is a non-receptor tyrosine kinase involved in the development and progression of cancer. However, the regulatory role of FAK in cell migration remains unclear. The aim of the present study was to investigate the mechanism underlying the regulation of melanoma cell migration by FAK. The effect of FAK knockdown on gene expression in B16F10 cells was examined by gene chip analysis. The expression levels of coiled-coil domain containing 80 (CCDC80) and epithelial (E)-cadherin were analyzed by reverse transcription quantitative polymerase chain reaction and western blotting. Wound healing and transwell assays were used to monitor B16F10 cell migration. It was identified that the knockdown of FAK increased the expression levels of CCDC80 and E-cadherin, while the overexpression of CCDC80 elevated E-cadherin expression. Concurrently, upregulation of CCDC80 inhibited the migration of B16F10 cells, and downregulation of CCDC80 promoted the migration of B16F10 cells. The clinical data from the Oncomine database also revealed that the mRNA level of FAK was increased while the mRNA levels of CCDC80 and E-cadherin were decreased in patients with melanoma compared with normal controls. Taken together, the results of the present study suggest that the regulation of B16F10 melanoma cell migration by FAK is potentially mediated by CCDC80.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.