ArticleOncotarget2018
YdjC chitooligosaccharide deacetylase homolog induces keratin reorganization in lung cancer cells: involvement of interaction between YDJC and CDC16.
Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 6 citations in OpenAlex.
- Downregulated genes by silencingAging · 2020Article
- Review
- YDJC Induces Epithelial-Mesenchymal Transition via Escaping from Interaction with CDC16 through Ubiquitination of PP2A.Journal of oncology · 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
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung cancer is a fatal disease with a high mortality rate. The perinuclear reorganization of keratin 8 (K8) is an important biochemical phenomenon reflecting changes in the physical properties of metastatic cancer. However, there is not much of information about the regulatory molecules involved in phosphorylation and perinuclear reorganization of K8. In this study, we investigated the role and molecular mechanisms of YdjC chitooligosaccha- ride deacetylase homolog (YDJC) in sphingosylphosphorylcholine (SPC)-induced phosphorylation and reorganization of K8, and migration and invasion (SPC-induced events). SPC induced expression of YDJC in a dose- and time-dependent manner. Gene silencing of YDJC suppressed SPC-induced events. YDJC overexpression induced the SPC-induced events. YDJC deacetylase dominant negative mutant (YDJCD13A) did not induce SPC-induced events. YDJC siRNA reduced ERK activation and overexpression of YDJC induced ERK activation. The siRNA of ERK1 or ERK2 suppressed YDJC-induced phosphorylation and reorganization of K8, and migration and invasion. Co-immunoprecipitation revealed that YDJC binds to CDC16. Interestingly, CDC16 siRNA induced SPC-induced events. Overexpression of CDC16 blocked SPC-induced events. KMPLOT analysis based on public microarray data revealed the poor prognosis of lung cancer patients with high expression of YDJC compared with patients with low expression of YDJC. The collective results indicate that YDJC is involved in SPC-induced events in A549 lung cancer cells by interacting with CDC16. YDJC overexpression might be involved in the progression of lung cancer. These results also suggest that suppression of YDJC or boosting of CDC16 interaction with YDJC might be a novel way to prevent progression of lung cancer.
Indexed as
Identifiers
What Socratic 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 Socratic graph.