ArticleDigestive diseases and sciences2019
Loss of Tyrosine Phosphatase Delta Promotes Gastric Cancer Progression via Signal Transducer and Activator of Transcription 3 Pathways.
Article in Digestive diseases and sciences, 2019. 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, 8 citations in OpenAlex.
- Striae gravidarum in the Han Chinese pregnant population: identifying genetic markers and risk factors through a prospective cohort study.BMC pregnancy and childbirth · 2025Article
- Article
- Protein Tyrosine Phosphatases: Mechanisms in Cancer.International journal of molecular sciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe protein tyrosine phosphatase delta (PTPRD) is a tumor suppressor, and its role in gastric cancer (GC) remains poorly understood.
methodsThe expressions of PTPRD were determined based on public data. In addition, the mRNA expressions of PTPRD in the GC samples, and the expressions of PTPRD in the GC cell lines including HGC27, SGC790, and BGC823, and gastric epithelial cell line GES-1 were determined by western blotting and quantitative real-time PCR. Furthermore, PTPRD siRNA was transfected into the HGC27 cell line, and then, cell proliferation, migration, and invasion were evaluated. The activity of signal transducer and activator of transcription 3 (STAT3) pathways in HGC27 cells transfected with PTPRD siRNA was determined by western blotting.
resultsPTPRD deletion was found in the GC patients, and this deletion was found to be correlated with poor prognosis in the GC patients. Expression of PTPRD was significantly downregulated in gastric carcinoma specimens and tumor cell lines when compared with those in normal controls. PTPRD also plays a key role in the GC cells proliferation, invasion, and migration. Silencing PTPRD expression by siRNA dramatically promoted GC cells proliferation, invasion, and migration. Mechanism study demonstrated that phosphorylation of STAT3 was inhibited by silencing PTPRD expression and the according changes including inhibition of cell migration and invasion were observed.
conclusionThis study supports PTPRD as a tumor suppressor and could be served as a marker for prognostic of GC. Silencing PTPRD could be a potential therapeutic in GC.
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.